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Effects of Daily Exogenous Oxytocin on Lactation Milk Yield and Composition
Effects of Daily Exogenous Oxytocin on Lactation Milk Yield and Composition S. D. NOSTRAND, D. M. GALTON, H. N. ERB,' and D. E. BAUMAN Department of Animal Science Cornel University Ithaca, NY 14853 ABSTRACT
Abbreviation key: IMI = intramammary infection, ME = mature equivalent, RCBD = randomized complete block design.
Eighty-four Holstein cows were used to determine effects of exogenous oxytocin on 305-<1 milk production and health. Cows were assigned at parturition by parity group to treatments: 1) oxytocin group, animals received an injection of I m1 (20 IU) of oxytocin at each milking throughout lactation and 2) control group, animals received no injection. Oxytocin injections were given in the thigh region within 3 min fonowing the initiation of udder preparation and immediately prior to machine attachment. Udder preparation consisted of forestripping and manual cleaning (10 to 20 s) and drying (5 to 10 s) of teats. Cows were milked in a parlor, and milk yield was recorded at each milking. Milk samples were conected from each cow biweekly for milk fat, protein, and somatic cell count determination. Individual lactations were modeled using Woods' lactation equation; resulting coefficients were analyzed using ANOVA. The oxytocin group produced 849 kg more milk during the lactation than the control group, with a significant difference occurring after peak milk yield. This suggests that exogenous oxytocin maintained greater persistency during lactation. No significant differences existed for milk fat or protein percentages. The use of exogenous oxytocin at milking increased lactation milk production with no apparent effect on health. (Key words: exogenous oxytocin, milk yield, health)
INTRODUCTION
Received Septembe£ 11, 1990. Accepted January 17, 1991. lDepartment of Clinical Sciences, New York State College of Veterinary Medicine. 1991 J Daily Sci 74:2119-2127
The discovery of oxytocin and the elucidation of its role in the neuro-hormonal milk ejection process allowed for managing the milking process with an exogenous hormone (9). Alterations in both milk and fat yield were obtained by milking a second time (immediately following the primary milking) with the aid of oxytocin. Results varied from significant increases in milk production (2, 16) and fat yield (8, 26) to no change in either milk yield (15, 18, 25) or fat yield (25). Disparate results can be explained by the varied experimental designs employed, with the majority of the work involving small sample sizes, alternating treatments, and short treatment periods. Variations in dosage and timing of injections have contributed to the confusion regarding effects of exogenous oxytocin. Studies have involved injections prior to hourly milking (8) or injections up to 1 h before milking (10). Such designs do not mimic nonnal physiology of lactation, in which oxytocin is released into the bloodstream due to normal milking stimuli, binds to myoepithelial cell receptors in the udder, and elicits milk ejection. Only a few studies (1, 27) administered oxytocin immediately prior to milking; increases in milk. production were reported when oxytocin administration occurred within minutes of a normal milking. Our study was designed to use exogenous oxytocin as a management tool without disruption of normal milking practices with injections occurring immediately prior to milking. Our objective was to determine the effect of long-term administration of exogenous oxytocin on milk. production, milk composition, and
2119
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NOSTRAND ET AL.
other associated parameters.
health
and
management
MATERIALS AND METHODS Animal selection ~ighty-four Holstein cows were randomly aSSIgned to treatments at parturition for a 305-<1 lactation production study. Animals were blocked by parity (primiparous and multiparous) and randomized in pairs by calving date. This procedure was used to balance treatments during the 8-mo assignment period in order to control for seasonal and management effects. At parturition, cows were evaluated for assi~~nt to the study on the basis of body condition, udder confrrmation, and health status. Cows were not used with 1) body condition score of less than 3 [scale of 1 to 5 (33)], 2) shape and depth of udder that may have in!erfered with milking practices and complete milk removal, or 3) a history of health disorm:rs. During the fIrst 3 wk postpartum, animals WIth expressed metabolic and other health disorders were excluded. Exclusions were for clinical ketosis, clinical milk fever, displaced abomasum, and presence of intramammary infections (IMI).
Treatments
Treatments were 1) oxytocin group animals received an injection of 1 ml (20 IU) of oxytocin ["Oxytocin Injection"; Butler Company, Rochester, NY; labeled dosage for milk letdown = .5 to 1.0 ml (10 to 20 IU)] at each milking and 2) control group, animals received no injec~on at milking. The control group did not receIVe placebo injections because the objective was not to detennine the efficacy of exogenous oxytocin but to study its use as a management practice. . ~sage of oxytocin was chosen to provide a nse m plasma concentration of oxytocin that would elicit a milk ejection response during the machine milking period. Subcutaneous and intramuscular injections of 20 IU oxytocin caused .milk ejection in 1.5 to 2 min (12, 22), a.nd reSIdual milk was obtained with Lm. injectIons of 20 ill (29). Based on this previous work and labeled dosage, a 20-1U Lm. dose Joumal of Dairy Science Vol. 74, No.7. 1991
was chosen. Oxytocin was administered immediately prior to machine attachment Injections (i.m.) were given with disposable individual 22-gauge needles and 3-ml syringes in the thigh region. Treatment began on the third to fifth milking after parturition and continued at every milking throughout the 305-<1 lactation. Treabnent was initiated during early lactation to maximize the effect of exogenous oxytocin on milk production. Management
Cows were milked together in a herringbone parlor. Premilking udder preparation consisted of forestripping (1 to 3 streams), washing teats with a wet paper towel (10 to 20 s), teat dipping with a .5% iodophor teat dip (Theratec; Babson Bros. Co., Naperville, ll..), and manual drying of teats with a dry paper towel (5 to 10 s). Oxytocin injections occurred immediately prior to machine attachment. Machine attachment occurred within 3 min of the initiation of udder preparation; majority of machines were attached within 1 min. The 3-min time allotment was used to represent the more normal variation in timing of machine attachment on many farms. Machine attachment occurred for the control cows in the normal milking routine because cows of both treatments were milked together. Machines were automatically removed upon cessation of milk flow (20 s). Postmilking teat dipping occurred after each milking with the same i~ophor teat dip used for premilking teat dippmg. Cows were housed together in free stalls bedded with sawdust. Total mixed rations were fed and formulated according to the university herd's average level of milk production based on DIM. In later lactation, cows were changed to a lower nutrient density ration if body condition score exceed 3+ to 4 -. Breeding began on first detected estrus after 60 DIM. Data Collection
Milk weights were recorded at each milking by the use of weigh jars. Biweekly milk samples for two consecutive milkings were taken for each cow. Samples were analyzed for fat, total protein, and somatic cell COWlt by DHIA. New IMI were confmned when one of the following criteria were met: 1) isolation of an
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EXOGENOUS OXYTOCIN AND MILK PERFORMANCE
organism from a milk sample taken from a clinical mastitis quarter or 2) isolation of an organism from at least two consecutive monthly milk samples. Quarter duplicate milk samples were taken aseptically every month for bacteriological determination in order to identify subclinical mastitis. A third milk sample was taken within 1 wk and cultured for confirmation of subclinical IMI if the duplicate samples differed Prior to antibiotic therapy of clinical mastitis, duplicate milk samples were taken for the determination of the causative organism. Microbiological procedures were in accordance with the National Mastitis Council (20). Animals were designated as mastitis positive if they had an incidence of clinical or subclinical mastitis due to a major pathogen that was verified by bacteriological culture. Cows showing clinical symptoms with bacteriologically negative culture were designated mastitis negative cows. Major pathogens included Staphylococcus aureus, Streptococcus species, Escherichia coli, Klebsiella, Pseudomonas, Pasteurella, Proteus, Serratia, yeast,
Nocardia, Prototheca, Corynebacterium pyogenes, and Enterobacter. Health and reproductive events were monitored by university herd health management personnel, including daily observation of cows for clinical signs of disease and estrus. The herd was on a routine herd health program. General health and reproductive information was obtained from individual cow health records. Statistical Analysis
For each cow, daily milk yields were convened to mean weekly milk weights. These data were used by least squares regression methods for modeling individual cow lactation curves by Wood's equation (32), which yields three coefficients that generally can be associated as a) initial height of the lactation curve, b) slope of the rising ponion of the lactation curve, and c) slope of the declining portion of the lactation curve. Lactation milk production response was analyzed by ANOVA of the Wood's equation coefficients. In addition, average fat percentage, protein percentage, and mature equivalent (ME) milk were used as dependent variables in the ANOVA. Mastitis was prevalent during the study; thus, mastitis infection may have interfered with the response to treatment. Therefore, mastitis was included as a separate treatment
factor in the analysis. This resulted in four treatment combinations, which were incorporated into each ANOVA as a 2 x 2 factorial treatment structure. The two factor levels are oxytocin treatment (oxytocin and control) and mastitis (+ or - incidence), which gives the treatments: oxytocin with mastitis, oxytocin without mastitis, control with mastitis, and control without mastitis. For each of the six dependent variables, an ANOVA was performed that incorporated the following model equation for a randomized complete block design (RCBD): Yijk = ~
+
Pj
+
Ti
+ (P x
nij
+
~jk
where
= milk yield as
modeled by Wood's parameters (a, b, or c), fat, protein, or ME milk. overall mean, ~ Pj = parity (primiparous, multiparous), Ti = treatment effect (oxytocin with mastitis, oxytocin without mastitis, control with mastitis, control without mastitis), and &jk = residual error.
Yijk
To test treatments, single degree of freedom contrasts were constructed from the least squares means. Contrast estimates were tested for significance against the mean square error of the parity by treatment interaction (which is implicitly assumed to be zero for an RCBD). These contrasts included tests for the oxytocin by mastitis interaction, the oxytocin effect, and the mastitis effect. If the oxytocin by mastitis interaction contrast was significant for one of the dependent variables, then for that variable only stratified simple effects were analyzed (i.e., oxytocin contrasts estimated within level of mastitis). If the oxytocin by mastitis interaction was nonsignificant, then the oxytocin treatment effect was estimated across the mastitis levels. All analyses were performed using SAS (24); ex = .10 was considered to be significantly different. RESULTS AND DISCUSSION Milk Production
Cows (n = 84) entered the study at the time of calving within an 8-mo period during which Jomnal of Dairy Science Vol. 74, No.7, 1991
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NOSTRAND ET AL.
TABLE 1. Test statistics for treatment contrasts and error terms. Composition
Wood's coefficients
a
Source
Fat
c
b
Protein
MEl Milk yield
- - - F statistic for treatment x parity for dependent variables - - -
Treatment x parity (contrast error term)
1.29
.99
Main effects Mastitis x oxytocin Oxytocin effect Mastitis effect Simple effects Oxytocin with mastitis Oxytocin without mastitis 1ME
.49
.54
.86
.49
Student's t statistic for all contrasts
Contrast
= Mature
-.30 1.13 -.83
1.07 .84 .07
2.66t
1.61 .44 3.31*
.52 .86 2.01
-2.07 4.75*** -.62
.04 4.00*
equivalent.
tP < .10. *p < .05. *"P < .025.
30% of the animals represented frrst and 70% second and greater lactations. Seventy-three cows (30% primiparous cows) with lactation records of greater than 150 DIM were used for data analysis. For these cows, number of lactations for control cows ranged from 1 to 9 with median and mode of 2.92 and 2, and number of lactations for oxytocin-treated cows ranged from 1 to 7 with median and mode of 2.51 and 2. Multiparous cows had a mean previous lactation ME of 9040 kg (SD = 1230) for the control group (n = 27) and 8550 kg (SD = 1350) for the oxytocin group (n = 24). First lactation animals had mean estimated producing ability of 1490 (SD = 760) for the control and 1310 (SD = 6(0) for the oxytocin-treated animals. Cows with greater than 150 DIM were used in order to have sufficient milk production data to predict the lactation curve for each cow by using Wood's lactation model. The Student's t statistic for contrasts on each dependent variable are shown in Table 1. The overall parity by treatment interaction was nonsignificant (P > .28) for all dependent variables, which supports the necessary assumption of no interaction for a RCBD design. Tests of the mastitis by oxytocin interaction contrast were nonsignificant (P > .1) for all variables with the exception of Wood's c coefficient, which was significant (P < .1). 1berefore, only simple effects were analyzed for the Journal of Dairy Science Vol. 74, No.7, 1991
c coefficient, and main effects were analyzed for all other variables. Simple effect contrasts of Wood's c coefficient were constructed for oxytocin treatment at each level of mastitis. Significance (P < .05) was observed for the c coefficient of the oxytocin treatments with no mastitis, but no significant effect (P > .5) was detected for cows with mastitis. No differences (P > .2) were detected among treatments for the a or b coefficients using main effects contrasts. Actual milk yield data were used to compute the age-season adjusted projected 305-d record (ME) for all cows. Least squares mean ME ± SE were significantly different (P < .025) and were 9609 ± 239 kg and 8588 ± 237 kg for the oxytocin-treated and control cows. The significance of coefficient c for cows unaffected by mastitis indicates that the use of exogenous oxytocin increased lactation milk production during the declining phase (after peak milk yield) of lactation. The nonsignificance of coefficients a and b indicates that either the use of exogenous oxytocin did not affect lactation milk yield during prepeak and peak milk yield periods or the difference was too small to be detected. This fmding is in agreement with earlier work (16, 17) perfonned with late lactation cows, which indicated that the use of exogenous oxytocin in-
2123
EXOGENOUS OXYTOCIN AND MILK PERFORMANCE 40
40
38 36
--.--
Control
.........goo-
Oxytocin
34
'" " ~
38
--
Control
36
~
Oxytocin
34
32
32
30
30
E
28 26
;;
Ii
24
-"
22
i
20
"Ii
28 26
;;
24
-"
22
i
20
18
18
16
16
14
14
12
12
10
10 0
10
15
20
25
30
35
40
45
50
0
10
15
Week of Lactation
Figure 1. Lactation curves by treatment derived from Wood's lactation model using least squares means for all cows.
creased milk yield after peak. production. Thus, oxytocin appears to have altered the slope of the declining phase of lactation. This effect was not observed when mastitis was present, which may be due to udder infections depressing milk yield during the declining phase of lactation. Although mastitis confounded the milk production analysis using Wood's model, the ME milk analysis was not confounded. The disparity between these results is explained by the nature of the lactation estimating techniques. The ME is an adjusted lactation production estimate that accounts for age and season of calving and, therefore, gives a general overview of the lactation. In contrast, the Wood's equation separates the lactation into its component parts without adjustment for age or season. The combination of the results of both the ME and Wood's coefficient analysis indicates that oxytocin treatment led to a significant increase in milk: yield. Lactation milk curves are in Figures 1, 2, and 3 for all cows and for cows with and without mastitis. These lactation curves represent the lactation milk yield as estimated by the adjusted mean coefficients from the Wood's lactation equation (Table 2). Differences in the estimated milk: production of the two treatment groups, regardless of mastitis status, ranged from 6.3 to 22.7% increase in milk production at wk 10 and 40. The mean lactation milk yield was 8162 and 7313 kg for
20
25
30
35
40
45
50
Week of lactation
Figure 2. Lactation curves by treatment derived from Wood's lactation model using least squares means for cows with mastitis.
oxytocin and control groups. This difference in milk: production represents an overall increase
of 11.6% for cows receiving exogenous oxytocin. Several mechanisms have been proposed to explain the effect of oxytocin on milk yield. Our data support the concept whereby oxytocin alters the involution process of alveoli during lactation. A decrease in the rate of secretory cell involution could explain the milk yield results obtained and the subsequent
40 38 36
--.--
Control
--0--
Oxytocin
34 32 30
'" ... ~
Ii
28 26
>:
24
:!!
22
:i
20 18 16 14 12 10 0
10
15
20
25
30
35
40
45
50
Week o. Lac1atlon
Figure 3. Lactation curves by treatment derived from Wood's 1actation model using least squares means for cows without mastitis. Journal of DaiIy Science Vol. 74, No.7, 1991
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NOSTRAND ET AL.
TABLE 2. Least squares means of Wood's coefficients for milk production and somatic cell linear scores by treatment and incidence of mastitis.
Treatments
Wood's coefficients
No. of cows
a
X
Somatic cell linear scores
c
b X
SE
X
SE
X
SE
.17 .19
.018 .018
.023 .029
.0022 .0023
2.43 2.58
.17
27.89 1.18 26.90 1.28
.182 .026 .0177 .028
.026 .026
.0033 .0036
3.00 3.19
.36 .32
2726 1.11 25.56 1.01
.158 .204
.020 .031
.0031 .0029
1.92
2.12
20 .16
All cows Oxytocin Control
35 38
27.58 26.23
Cows with mastitis Oxytocin Control
17 16
Cows without mastitis Oxytocin Control
18 22
SE .81 .82
change in the slope of the lactation curve. This mechanism is supported by studies with rats (28) and mice (6), in which biochemical and histological evidence suggested that oxytocin can maintain secretory cell integrity during late lactation. Rather than a direct effect on the secretory tissue, exogenous oxytocin may simply be preventing a normal decline in milk yield due to changes in endogenous oxytocin secretion. Wachs et al. (31) suggested that the sensitivity of the neuroendocrine reflex declines with advancing lactation. Therefore, less hormone is available for milk ejection as lactation progresses. This could result in decreased stimulus to eject milk and in an increase in the onset of alveolar involution. There was no sudden increase in milk pr0duction of treated cows with our data, but rather a slow increase in production as lactation progressed. However, the design in this study did not allow for the detection of a sudden increase in milk production because the use of exogenous oxytocin started soon after calving. Thus, a mechanism that can not be directly inferred from our data is that exogenous oxytocin may allow for a more complete evacuation of milk from the udder at each milking (sudden production increase), thereby lowering intramammary pressure, which may allow greater secretory activity between milkings. Evidence to support the udder evacuation mechanism is reported in the literature (4, 17, 21, 30). Alternatively, Henderson (14) indicated that secretion in goats may be limited by feedback Journal of Dairy Science Vol. 74, No.7, 1991
.025 .022
.18
from an unidentified chemical in the milk rather than by internal alveolar pressure. Tucker (30) suggested chemical feedback as a possibility in cows. Whether the limitation is due to intramammary pressure or chemical feedback, oxytocin may act to lower the amount of residual milk in the alveoli, thus decreasing the stimulus to lower secretion rate. Brandsma (5) reported that decreasing the amount of residual milk left in the udder after normal milking (by the use of exogenous oxytocin) resulted in an increase in milk production during the later part of lactation compared with cows without residual milk removed. Similar changes in milk yield (13 to 17%) were seen with increases in milking frequency (three times milking) (7). Thus, a reduction in the amount of milk left in the udder appears to influence total production. Although data from this study do not support mechanisms that produce an immediate change in volwne of secretion, small increases in milk yield during early lactation may not have been detectable with the treatment regimen. Therefore, these mechanisms remain plausible. If the onset of oxytocin treatment had been delayed, an initial step increase in milk yield may have been observed. The actual mechanism of exogenous oxytocin on milk production may be a combination of the reversal of the decrease in hormonal sensitivity and lowering of pressure or chemical feedback. Along with consideration of the possible mechanisms, the time interval between initiation of udder preparation and machine attachment may have a potential effect on milk
2125
EXOGENOUS OXYTOCIN AND Mll..K. PERFORMANCE TABLE 3. Number of new intramammary infections by cow and by treatment. Number of new intramammary infections by cow Treatment Oxytocin Control
Staphylococcus aureus
No. of total cows
Streptococcus
I
35
o
38
species
Environmental organisml
7
8
I
4
7
5
=
lEnvironmental organism Escherichia coli, Klebsiella. and Pseudomonas. Other yeast, Nocardia, Prototheca, Corynebacterium pyogenes, and Enterobacter.
2ainicaI
Total
Other
= Pasteurella, Proteus, Serratia,
mastitis with a bacteriological isolate.
production. The long-standing recommendation has been a I-min interval for continuous stimulation or 30 s of stimulation followed by 30 s of delay before machine attachment to achieve optimal milk ejection; however, recent findings indicate that this treatment may not be as necessary or that the degree of benefit may not be as great with high producing cows and modem milking equipment (11, 19, 23, 31). A recent lactation study (19) indicated no statistical difference for lactation milk yield with full stimulation, a 60-s routine, compared with a minimum stimulation, a 15-s routine, before machine attachment. In our study, machines were attached within 3 min after the initiation of a good udder preparation, with most machines attached within I min. Machine attachment varied for all cows at each milking because the treatment groups were milked together, and cows entered the parlor in a random order. Additional research is warranted to determine the possible interaction for the timing of machine attachment with and without the use of exogenous oxytocin. Milk Composition
Overall mean fat and protein percentages did not differ (P > .40) for oxytocin and
control cows during lactation. Fat averaged 3.59% ± .066 and 3.61 % ± .067 and protein 3.11% ± .040 and 3.15% ± .040 for oxytocin and control cows. Changes in milk fat content reported by others during short-term experiments (8, 11, 23, 26) were not seen in this full lactation study. The results suggest that chronic use of oxytocin does not alter milk content of fat and protein. However, production of total quantity of milk fat and milk protein varied proportionally with changes in lactation milk yield. Health No significant differences (P > .10) existed for somatic cell linear scores by treatment (fable 2). Numbers of cows by treatment and type of mastitis organisms are in Table 3. Number of total cows determined to have mastitis (both subclinical mastitis and clinical mastitis with an isolate) was 17 and 16 for oxytocin group and controls. Cows showing clinical signs with negative bacteriological culture numbered 4 for the oxytocin group and 1 for the control group. Although the presence of mastitis appeared to cause a nonresponse to exogenous oxytocin, the use of exogenous oxytocin did not appear to affect the incidence
TABLE 4. Reproductive parameters for all cows by treatment.
Treatment
cows
No. of pregnant cows
Oxytocin
35
28
7
Co~
~
~
9
No. of
No. of cows not
pregnant
Days openl
X
SD
136.7 130.0
58 54
IPregnant cows only; pregnant cows conf"mned by rectal palpation during lactation. Journal of Dairy Science Vol. 74, No.7, 1991
2126
NOSTRAND ET AL.
of mastitis, as evidenced by the even distribution of infections between groups and by the nonsignificance of the somatic cell linear scores. Previous work (3, 13) has shown that the use of exogenous oxytocin may affect the length of the estrous cycle when administered at 100 IU/d or greater. In this study, cows received 20 IU at each milking twice daily, and no apparent detrimental effects were observed (Table 4). No unfavorable reactions were noted to the twice daily injections. Several cows exhibited increased anxiety during udder preparation early in the study; however, cows adjusted within a few weeks. No abscesses were detected at the site of injections. CONCLUSIONS
Administration of exogenous oxytocin to cows for a full lactation increased milk yield by 11.6% over cows not receiving oxytocin, but no alteration in milk composition or apparent difference in reproductive or health parameters occurred. It appears that most of the increase in milk yield occurred during the declining phase of lactation. Possible mechanisms for this action were proposed, but future research is needed to understand these mechanisms and the importance of timing of machine attachment relative to initiation of udder preparation. Mastitis appeared to negate the effect of oxytocin administration. Warning
The use of exogenous oxytocin in herds for milk production reasons is presently prohibited
by the United States Food and Drug Administration; thus, its use as a management tool is illegal and not recommended. REFERENCES 1 Adams. H. P., and N. N. Allen. 1952. The value of oxytocin for reducing fluctuations in milk and fat yield. J. Dairy Sci. 35:1117. 2 Adams, H. P., and N. N. Allen. 1952. The effect of removal of residual milk by use of oxytocin upon the yield and fat content of subsequent milkings. J. Dairy Sci. 35:1121. 3 Armstrong. D. T.• and W. Hansel. 1959. Alteration of the bovine estrous cycle with oxytocin. J. Dairy Sci. 42:533. Journal of Dairy Science Vol. 74, No.7, 1991
4Benson, G. K., and S. J. Folley. 1957. The effect of oxytocin on mammary gland involution in the mt. J. Endocrinol. 16:189. 5 Brandsma, S. 1978. The relation between milking. residual milk and milk yield. Page 47 in Proc. Int. Symp. Machine Milking, Louisville, KY, Natl. Mastitis COUIlC., Washington, DC. 6 CaruoIo, E. V. 1971. Exogenous oxytocin and lactation in the mouse. J. Dairy Sci. 54:1207. 7 DcPeters, E. J., N. E. Smith, and J. Acedo-Rico. 1985. Three or two times daily milking of older cows and first lactation cows for entire lactations. J. Dairy Sci. 68:123. 8 Donker, J. D., J. H. Koshi, and W. E. Petersen. 1954. The effects of hourly milking with the aid of intravenous injection of oxytocin. J. Dairy Sci. 37:1261. 9 Ely, F., and W. E. Petersen. 1941. Factors involved in the ejection of milk. J. Dairy Sci. 24:211. 10 Gavin, W. 1913. On the effects of administration of extracts of pituitary body and corpus luteum to milch cows. Q. J. Exp. Physiol. 6:13. 11 Gorewit, R C., and R Sagi. 1984. Effects of exogenous oxytocin on production and milking variables of cows. J. Dairy Sci. 67:2050. 12 Graf, G. C. 1968. Effects of oxytocin injected intramuscularly and intravenously on milk ejection of bovine. J. Dairy Sci. 51(SuppI. 1):628.(Abstr.) 13 Hansel, W., and W. C. Wagner. 1960. Luteal inhibition in the bovine as a result of oxytocin injections, uterine dilatation, and intrauterine infusions of seminal and preputial fluids. J. Dairy Sci. 43:796. 14 Henderson, A. J., and M. Peaker. 1984. Feed-back control of milk secretion in the goat by a chemical in milk. J. Physiol. 351:39. 15 Hill, R. L., and S. Simpson. 1914. The effect of pituitary extract on the secretion of milk in the cow. Proc. Soc. Exp. BioI. Med. 11:82. 16 Knodt, C. B., and W. E. Petersen. 1942. The effect of the continuous injection of pitocin upon milk and milk fat production. J. Dairy Sci. 25:709. 17Knodl, C. B., and W. E. Petersen. 1944. The effect of complete evacuation of the mammary gland by pitocin upon milk and fat production. J. Dairy Sci. 27:449. 18 Koshi, J. H.• and W. E. Petersen. 1955. Complementary milk and its relationship to lactation. J. Dairy Sci. 38:788. 19 Merrill, W. G., R. Sagi, L. G. Petersson, T. V. Bui, H. N. Erb, D. M. Galton, and R. Gates. 1987. Effects of premilking stimulation on complete lactation milk yield and milking performance. J. Dairy Sci. 70:1676. 20 National Mastitis Council. 1981. Microbiological procedures for usc in the diagnosis of bovine mastitis. Natl. Mastitis Counc., Washington, DC. 21 Petersen, W. E., and T. V. Rigor. 1932. Relation of pressure to mte and quality of milk secreted. Proc. Soc. Exp. BioI. MOO. 30:254. 22 Premachandra, B. N., G. W. Pipes, and R. von Bersvordt-Wallmbe. 1959. Comparison of the intravenous and subcutaneous injections of oxytocin in the lactating cow. J. Dairy Sci. 42:918. 23 Sagi, R., R. C. Gorewil, and D. B. Wilson. 1980. Role of exogeDOns oxytocin in eliciting milk ejection in dairy cows. J. Dairy Sci. 63:2006.
EXOGENOUS OXYTOCIN AND MILK PERFORMANCE
24 SAS® User's Guide: Statistics, Version 5 Edition. 1985. SAS Inst, Inc., Cary, NC. 25 Shaw, J. C. 1942. The effect of oxytocin on milk and milk fat secretion. 1. Dairy Sci. 25:1051. 26 Smith, V. R. 1947. The effect of milking at short intervals with and without injections of oxytocin. 1. Dairy Sci. 30:703. 27 Sprain, D. G., V. R. Smith, W. 1. Tyler, and O. T. Fosgate. 1954. The effect on milk and fat production of injections of oxytocin at alternate 14-day periods during lactation. 1. Dairy Sci. 37:195. 28 Thatcher, W. W., and H. A. Tucker. 1970. Lactational performance of rats injected with oxytocin, cortisol21-acetate, prolactin, and growth hormone during prolonged lactation. Endocrinology 86:237. 29 Thompson, P. D., M. 1. Paape, and J. W. Smith. 1973.
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Residual milk yield as affected by dose and time of injection of oxytocin. J. Dairy Res. 40:221. 30 Tucker, H. A., R. P. Reece, and R. E. Mather. 1961. Udder capacity estimates as affected by rate of milk secretion and intramammary pressure. J. Dairy Sci. 44:1725. 31 Wachs, E. A., R C. Gorewit, and W. B. Currie. 1984. Oxytocin concentration of cattle in response to milking stimuli through lactation and mammary involution. Domest. Anim. Endocrinol. 1:141. 32 Wood, P.D.P. 1967. Algebraic model of the lactation curve in cattle. Nature (Lond.) 216:164. 33 Wildman, E. E., G. M. lones, P. E. Wagner, and R. L. Boman. 1982. A dairy cow body condition scoring system and its relationship to selected production characteristics. J. Dairy Sci. 65:495.
Journal of Dairy Science Vol. 74, No.7, 1991
Abbreviation key: IMI = intramammary infection, ME = mature equivalent, RCBD = randomized complete block design.
Eighty-four Holstein cows were used to determine effects of exogenous oxytocin on 305-<1 milk production and health. Cows were assigned at parturition by parity group to treatments: 1) oxytocin group, animals received an injection of I m1 (20 IU) of oxytocin at each milking throughout lactation and 2) control group, animals received no injection. Oxytocin injections were given in the thigh region within 3 min fonowing the initiation of udder preparation and immediately prior to machine attachment. Udder preparation consisted of forestripping and manual cleaning (10 to 20 s) and drying (5 to 10 s) of teats. Cows were milked in a parlor, and milk yield was recorded at each milking. Milk samples were conected from each cow biweekly for milk fat, protein, and somatic cell count determination. Individual lactations were modeled using Woods' lactation equation; resulting coefficients were analyzed using ANOVA. The oxytocin group produced 849 kg more milk during the lactation than the control group, with a significant difference occurring after peak milk yield. This suggests that exogenous oxytocin maintained greater persistency during lactation. No significant differences existed for milk fat or protein percentages. The use of exogenous oxytocin at milking increased lactation milk production with no apparent effect on health. (Key words: exogenous oxytocin, milk yield, health)
INTRODUCTION
Received Septembe£ 11, 1990. Accepted January 17, 1991. lDepartment of Clinical Sciences, New York State College of Veterinary Medicine. 1991 J Daily Sci 74:2119-2127
The discovery of oxytocin and the elucidation of its role in the neuro-hormonal milk ejection process allowed for managing the milking process with an exogenous hormone (9). Alterations in both milk and fat yield were obtained by milking a second time (immediately following the primary milking) with the aid of oxytocin. Results varied from significant increases in milk production (2, 16) and fat yield (8, 26) to no change in either milk yield (15, 18, 25) or fat yield (25). Disparate results can be explained by the varied experimental designs employed, with the majority of the work involving small sample sizes, alternating treatments, and short treatment periods. Variations in dosage and timing of injections have contributed to the confusion regarding effects of exogenous oxytocin. Studies have involved injections prior to hourly milking (8) or injections up to 1 h before milking (10). Such designs do not mimic nonnal physiology of lactation, in which oxytocin is released into the bloodstream due to normal milking stimuli, binds to myoepithelial cell receptors in the udder, and elicits milk ejection. Only a few studies (1, 27) administered oxytocin immediately prior to milking; increases in milk. production were reported when oxytocin administration occurred within minutes of a normal milking. Our study was designed to use exogenous oxytocin as a management tool without disruption of normal milking practices with injections occurring immediately prior to milking. Our objective was to determine the effect of long-term administration of exogenous oxytocin on milk. production, milk composition, and
2119
2120
NOSTRAND ET AL.
other associated parameters.
health
and
management
MATERIALS AND METHODS Animal selection ~ighty-four Holstein cows were randomly aSSIgned to treatments at parturition for a 305-<1 lactation production study. Animals were blocked by parity (primiparous and multiparous) and randomized in pairs by calving date. This procedure was used to balance treatments during the 8-mo assignment period in order to control for seasonal and management effects. At parturition, cows were evaluated for assi~~nt to the study on the basis of body condition, udder confrrmation, and health status. Cows were not used with 1) body condition score of less than 3 [scale of 1 to 5 (33)], 2) shape and depth of udder that may have in!erfered with milking practices and complete milk removal, or 3) a history of health disorm:rs. During the fIrst 3 wk postpartum, animals WIth expressed metabolic and other health disorders were excluded. Exclusions were for clinical ketosis, clinical milk fever, displaced abomasum, and presence of intramammary infections (IMI).
Treatments
Treatments were 1) oxytocin group animals received an injection of 1 ml (20 IU) of oxytocin ["Oxytocin Injection"; Butler Company, Rochester, NY; labeled dosage for milk letdown = .5 to 1.0 ml (10 to 20 IU)] at each milking and 2) control group, animals received no injec~on at milking. The control group did not receIVe placebo injections because the objective was not to detennine the efficacy of exogenous oxytocin but to study its use as a management practice. . ~sage of oxytocin was chosen to provide a nse m plasma concentration of oxytocin that would elicit a milk ejection response during the machine milking period. Subcutaneous and intramuscular injections of 20 IU oxytocin caused .milk ejection in 1.5 to 2 min (12, 22), a.nd reSIdual milk was obtained with Lm. injectIons of 20 ill (29). Based on this previous work and labeled dosage, a 20-1U Lm. dose Joumal of Dairy Science Vol. 74, No.7. 1991
was chosen. Oxytocin was administered immediately prior to machine attachment Injections (i.m.) were given with disposable individual 22-gauge needles and 3-ml syringes in the thigh region. Treatment began on the third to fifth milking after parturition and continued at every milking throughout the 305-<1 lactation. Treabnent was initiated during early lactation to maximize the effect of exogenous oxytocin on milk production. Management
Cows were milked together in a herringbone parlor. Premilking udder preparation consisted of forestripping (1 to 3 streams), washing teats with a wet paper towel (10 to 20 s), teat dipping with a .5% iodophor teat dip (Theratec; Babson Bros. Co., Naperville, ll..), and manual drying of teats with a dry paper towel (5 to 10 s). Oxytocin injections occurred immediately prior to machine attachment. Machine attachment occurred within 3 min of the initiation of udder preparation; majority of machines were attached within 1 min. The 3-min time allotment was used to represent the more normal variation in timing of machine attachment on many farms. Machine attachment occurred for the control cows in the normal milking routine because cows of both treatments were milked together. Machines were automatically removed upon cessation of milk flow (20 s). Postmilking teat dipping occurred after each milking with the same i~ophor teat dip used for premilking teat dippmg. Cows were housed together in free stalls bedded with sawdust. Total mixed rations were fed and formulated according to the university herd's average level of milk production based on DIM. In later lactation, cows were changed to a lower nutrient density ration if body condition score exceed 3+ to 4 -. Breeding began on first detected estrus after 60 DIM. Data Collection
Milk weights were recorded at each milking by the use of weigh jars. Biweekly milk samples for two consecutive milkings were taken for each cow. Samples were analyzed for fat, total protein, and somatic cell COWlt by DHIA. New IMI were confmned when one of the following criteria were met: 1) isolation of an
2121
EXOGENOUS OXYTOCIN AND MILK PERFORMANCE
organism from a milk sample taken from a clinical mastitis quarter or 2) isolation of an organism from at least two consecutive monthly milk samples. Quarter duplicate milk samples were taken aseptically every month for bacteriological determination in order to identify subclinical mastitis. A third milk sample was taken within 1 wk and cultured for confirmation of subclinical IMI if the duplicate samples differed Prior to antibiotic therapy of clinical mastitis, duplicate milk samples were taken for the determination of the causative organism. Microbiological procedures were in accordance with the National Mastitis Council (20). Animals were designated as mastitis positive if they had an incidence of clinical or subclinical mastitis due to a major pathogen that was verified by bacteriological culture. Cows showing clinical symptoms with bacteriologically negative culture were designated mastitis negative cows. Major pathogens included Staphylococcus aureus, Streptococcus species, Escherichia coli, Klebsiella, Pseudomonas, Pasteurella, Proteus, Serratia, yeast,
Nocardia, Prototheca, Corynebacterium pyogenes, and Enterobacter. Health and reproductive events were monitored by university herd health management personnel, including daily observation of cows for clinical signs of disease and estrus. The herd was on a routine herd health program. General health and reproductive information was obtained from individual cow health records. Statistical Analysis
For each cow, daily milk yields were convened to mean weekly milk weights. These data were used by least squares regression methods for modeling individual cow lactation curves by Wood's equation (32), which yields three coefficients that generally can be associated as a) initial height of the lactation curve, b) slope of the rising ponion of the lactation curve, and c) slope of the declining portion of the lactation curve. Lactation milk production response was analyzed by ANOVA of the Wood's equation coefficients. In addition, average fat percentage, protein percentage, and mature equivalent (ME) milk were used as dependent variables in the ANOVA. Mastitis was prevalent during the study; thus, mastitis infection may have interfered with the response to treatment. Therefore, mastitis was included as a separate treatment
factor in the analysis. This resulted in four treatment combinations, which were incorporated into each ANOVA as a 2 x 2 factorial treatment structure. The two factor levels are oxytocin treatment (oxytocin and control) and mastitis (+ or - incidence), which gives the treatments: oxytocin with mastitis, oxytocin without mastitis, control with mastitis, and control without mastitis. For each of the six dependent variables, an ANOVA was performed that incorporated the following model equation for a randomized complete block design (RCBD): Yijk = ~
+
Pj
+
Ti
+ (P x
nij
+
~jk
where
= milk yield as
modeled by Wood's parameters (a, b, or c), fat, protein, or ME milk. overall mean, ~ Pj = parity (primiparous, multiparous), Ti = treatment effect (oxytocin with mastitis, oxytocin without mastitis, control with mastitis, control without mastitis), and &jk = residual error.
Yijk
To test treatments, single degree of freedom contrasts were constructed from the least squares means. Contrast estimates were tested for significance against the mean square error of the parity by treatment interaction (which is implicitly assumed to be zero for an RCBD). These contrasts included tests for the oxytocin by mastitis interaction, the oxytocin effect, and the mastitis effect. If the oxytocin by mastitis interaction contrast was significant for one of the dependent variables, then for that variable only stratified simple effects were analyzed (i.e., oxytocin contrasts estimated within level of mastitis). If the oxytocin by mastitis interaction was nonsignificant, then the oxytocin treatment effect was estimated across the mastitis levels. All analyses were performed using SAS (24); ex = .10 was considered to be significantly different. RESULTS AND DISCUSSION Milk Production
Cows (n = 84) entered the study at the time of calving within an 8-mo period during which Jomnal of Dairy Science Vol. 74, No.7, 1991
2122
NOSTRAND ET AL.
TABLE 1. Test statistics for treatment contrasts and error terms. Composition
Wood's coefficients
a
Source
Fat
c
b
Protein
MEl Milk yield
- - - F statistic for treatment x parity for dependent variables - - -
Treatment x parity (contrast error term)
1.29
.99
Main effects Mastitis x oxytocin Oxytocin effect Mastitis effect Simple effects Oxytocin with mastitis Oxytocin without mastitis 1ME
.49
.54
.86
.49
Student's t statistic for all contrasts
Contrast
= Mature
-.30 1.13 -.83
1.07 .84 .07
2.66t
1.61 .44 3.31*
.52 .86 2.01
-2.07 4.75*** -.62
.04 4.00*
equivalent.
tP < .10. *p < .05. *"P < .025.
30% of the animals represented frrst and 70% second and greater lactations. Seventy-three cows (30% primiparous cows) with lactation records of greater than 150 DIM were used for data analysis. For these cows, number of lactations for control cows ranged from 1 to 9 with median and mode of 2.92 and 2, and number of lactations for oxytocin-treated cows ranged from 1 to 7 with median and mode of 2.51 and 2. Multiparous cows had a mean previous lactation ME of 9040 kg (SD = 1230) for the control group (n = 27) and 8550 kg (SD = 1350) for the oxytocin group (n = 24). First lactation animals had mean estimated producing ability of 1490 (SD = 760) for the control and 1310 (SD = 6(0) for the oxytocin-treated animals. Cows with greater than 150 DIM were used in order to have sufficient milk production data to predict the lactation curve for each cow by using Wood's lactation model. The Student's t statistic for contrasts on each dependent variable are shown in Table 1. The overall parity by treatment interaction was nonsignificant (P > .28) for all dependent variables, which supports the necessary assumption of no interaction for a RCBD design. Tests of the mastitis by oxytocin interaction contrast were nonsignificant (P > .1) for all variables with the exception of Wood's c coefficient, which was significant (P < .1). 1berefore, only simple effects were analyzed for the Journal of Dairy Science Vol. 74, No.7, 1991
c coefficient, and main effects were analyzed for all other variables. Simple effect contrasts of Wood's c coefficient were constructed for oxytocin treatment at each level of mastitis. Significance (P < .05) was observed for the c coefficient of the oxytocin treatments with no mastitis, but no significant effect (P > .5) was detected for cows with mastitis. No differences (P > .2) were detected among treatments for the a or b coefficients using main effects contrasts. Actual milk yield data were used to compute the age-season adjusted projected 305-d record (ME) for all cows. Least squares mean ME ± SE were significantly different (P < .025) and were 9609 ± 239 kg and 8588 ± 237 kg for the oxytocin-treated and control cows. The significance of coefficient c for cows unaffected by mastitis indicates that the use of exogenous oxytocin increased lactation milk production during the declining phase (after peak milk yield) of lactation. The nonsignificance of coefficients a and b indicates that either the use of exogenous oxytocin did not affect lactation milk yield during prepeak and peak milk yield periods or the difference was too small to be detected. This fmding is in agreement with earlier work (16, 17) perfonned with late lactation cows, which indicated that the use of exogenous oxytocin in-
2123
EXOGENOUS OXYTOCIN AND MILK PERFORMANCE 40
40
38 36
--.--
Control
.........goo-
Oxytocin
34
'" " ~
38
--
Control
36
~
Oxytocin
34
32
32
30
30
E
28 26
;;
Ii
24
-"
22
i
20
"Ii
28 26
;;
24
-"
22
i
20
18
18
16
16
14
14
12
12
10
10 0
10
15
20
25
30
35
40
45
50
0
10
15
Week of Lactation
Figure 1. Lactation curves by treatment derived from Wood's lactation model using least squares means for all cows.
creased milk yield after peak. production. Thus, oxytocin appears to have altered the slope of the declining phase of lactation. This effect was not observed when mastitis was present, which may be due to udder infections depressing milk yield during the declining phase of lactation. Although mastitis confounded the milk production analysis using Wood's model, the ME milk analysis was not confounded. The disparity between these results is explained by the nature of the lactation estimating techniques. The ME is an adjusted lactation production estimate that accounts for age and season of calving and, therefore, gives a general overview of the lactation. In contrast, the Wood's equation separates the lactation into its component parts without adjustment for age or season. The combination of the results of both the ME and Wood's coefficient analysis indicates that oxytocin treatment led to a significant increase in milk: yield. Lactation milk curves are in Figures 1, 2, and 3 for all cows and for cows with and without mastitis. These lactation curves represent the lactation milk yield as estimated by the adjusted mean coefficients from the Wood's lactation equation (Table 2). Differences in the estimated milk: production of the two treatment groups, regardless of mastitis status, ranged from 6.3 to 22.7% increase in milk production at wk 10 and 40. The mean lactation milk yield was 8162 and 7313 kg for
20
25
30
35
40
45
50
Week of lactation
Figure 2. Lactation curves by treatment derived from Wood's lactation model using least squares means for cows with mastitis.
oxytocin and control groups. This difference in milk: production represents an overall increase
of 11.6% for cows receiving exogenous oxytocin. Several mechanisms have been proposed to explain the effect of oxytocin on milk yield. Our data support the concept whereby oxytocin alters the involution process of alveoli during lactation. A decrease in the rate of secretory cell involution could explain the milk yield results obtained and the subsequent
40 38 36
--.--
Control
--0--
Oxytocin
34 32 30
'" ... ~
Ii
28 26
>:
24
:!!
22
:i
20 18 16 14 12 10 0
10
15
20
25
30
35
40
45
50
Week o. Lac1atlon
Figure 3. Lactation curves by treatment derived from Wood's 1actation model using least squares means for cows without mastitis. Journal of DaiIy Science Vol. 74, No.7, 1991
2124
NOSTRAND ET AL.
TABLE 2. Least squares means of Wood's coefficients for milk production and somatic cell linear scores by treatment and incidence of mastitis.
Treatments
Wood's coefficients
No. of cows
a
X
Somatic cell linear scores
c
b X
SE
X
SE
X
SE
.17 .19
.018 .018
.023 .029
.0022 .0023
2.43 2.58
.17
27.89 1.18 26.90 1.28
.182 .026 .0177 .028
.026 .026
.0033 .0036
3.00 3.19
.36 .32
2726 1.11 25.56 1.01
.158 .204
.020 .031
.0031 .0029
1.92
2.12
20 .16
All cows Oxytocin Control
35 38
27.58 26.23
Cows with mastitis Oxytocin Control
17 16
Cows without mastitis Oxytocin Control
18 22
SE .81 .82
change in the slope of the lactation curve. This mechanism is supported by studies with rats (28) and mice (6), in which biochemical and histological evidence suggested that oxytocin can maintain secretory cell integrity during late lactation. Rather than a direct effect on the secretory tissue, exogenous oxytocin may simply be preventing a normal decline in milk yield due to changes in endogenous oxytocin secretion. Wachs et al. (31) suggested that the sensitivity of the neuroendocrine reflex declines with advancing lactation. Therefore, less hormone is available for milk ejection as lactation progresses. This could result in decreased stimulus to eject milk and in an increase in the onset of alveolar involution. There was no sudden increase in milk pr0duction of treated cows with our data, but rather a slow increase in production as lactation progressed. However, the design in this study did not allow for the detection of a sudden increase in milk production because the use of exogenous oxytocin started soon after calving. Thus, a mechanism that can not be directly inferred from our data is that exogenous oxytocin may allow for a more complete evacuation of milk from the udder at each milking (sudden production increase), thereby lowering intramammary pressure, which may allow greater secretory activity between milkings. Evidence to support the udder evacuation mechanism is reported in the literature (4, 17, 21, 30). Alternatively, Henderson (14) indicated that secretion in goats may be limited by feedback Journal of Dairy Science Vol. 74, No.7, 1991
.025 .022
.18
from an unidentified chemical in the milk rather than by internal alveolar pressure. Tucker (30) suggested chemical feedback as a possibility in cows. Whether the limitation is due to intramammary pressure or chemical feedback, oxytocin may act to lower the amount of residual milk in the alveoli, thus decreasing the stimulus to lower secretion rate. Brandsma (5) reported that decreasing the amount of residual milk left in the udder after normal milking (by the use of exogenous oxytocin) resulted in an increase in milk production during the later part of lactation compared with cows without residual milk removed. Similar changes in milk yield (13 to 17%) were seen with increases in milking frequency (three times milking) (7). Thus, a reduction in the amount of milk left in the udder appears to influence total production. Although data from this study do not support mechanisms that produce an immediate change in volwne of secretion, small increases in milk yield during early lactation may not have been detectable with the treatment regimen. Therefore, these mechanisms remain plausible. If the onset of oxytocin treatment had been delayed, an initial step increase in milk yield may have been observed. The actual mechanism of exogenous oxytocin on milk production may be a combination of the reversal of the decrease in hormonal sensitivity and lowering of pressure or chemical feedback. Along with consideration of the possible mechanisms, the time interval between initiation of udder preparation and machine attachment may have a potential effect on milk
2125
EXOGENOUS OXYTOCIN AND Mll..K. PERFORMANCE TABLE 3. Number of new intramammary infections by cow and by treatment. Number of new intramammary infections by cow Treatment Oxytocin Control
Staphylococcus aureus
No. of total cows
Streptococcus
I
35
o
38
species
Environmental organisml
7
8
I
4
7
5
=
lEnvironmental organism Escherichia coli, Klebsiella. and Pseudomonas. Other yeast, Nocardia, Prototheca, Corynebacterium pyogenes, and Enterobacter.
2ainicaI
Total
Other
= Pasteurella, Proteus, Serratia,
mastitis with a bacteriological isolate.
production. The long-standing recommendation has been a I-min interval for continuous stimulation or 30 s of stimulation followed by 30 s of delay before machine attachment to achieve optimal milk ejection; however, recent findings indicate that this treatment may not be as necessary or that the degree of benefit may not be as great with high producing cows and modem milking equipment (11, 19, 23, 31). A recent lactation study (19) indicated no statistical difference for lactation milk yield with full stimulation, a 60-s routine, compared with a minimum stimulation, a 15-s routine, before machine attachment. In our study, machines were attached within 3 min after the initiation of a good udder preparation, with most machines attached within I min. Machine attachment varied for all cows at each milking because the treatment groups were milked together, and cows entered the parlor in a random order. Additional research is warranted to determine the possible interaction for the timing of machine attachment with and without the use of exogenous oxytocin. Milk Composition
Overall mean fat and protein percentages did not differ (P > .40) for oxytocin and
control cows during lactation. Fat averaged 3.59% ± .066 and 3.61 % ± .067 and protein 3.11% ± .040 and 3.15% ± .040 for oxytocin and control cows. Changes in milk fat content reported by others during short-term experiments (8, 11, 23, 26) were not seen in this full lactation study. The results suggest that chronic use of oxytocin does not alter milk content of fat and protein. However, production of total quantity of milk fat and milk protein varied proportionally with changes in lactation milk yield. Health No significant differences (P > .10) existed for somatic cell linear scores by treatment (fable 2). Numbers of cows by treatment and type of mastitis organisms are in Table 3. Number of total cows determined to have mastitis (both subclinical mastitis and clinical mastitis with an isolate) was 17 and 16 for oxytocin group and controls. Cows showing clinical signs with negative bacteriological culture numbered 4 for the oxytocin group and 1 for the control group. Although the presence of mastitis appeared to cause a nonresponse to exogenous oxytocin, the use of exogenous oxytocin did not appear to affect the incidence
TABLE 4. Reproductive parameters for all cows by treatment.
Treatment
cows
No. of pregnant cows
Oxytocin
35
28
7
Co~
~
~
9
No. of
No. of cows not
pregnant
Days openl
X
SD
136.7 130.0
58 54
IPregnant cows only; pregnant cows conf"mned by rectal palpation during lactation. Journal of Dairy Science Vol. 74, No.7, 1991
2126
NOSTRAND ET AL.
of mastitis, as evidenced by the even distribution of infections between groups and by the nonsignificance of the somatic cell linear scores. Previous work (3, 13) has shown that the use of exogenous oxytocin may affect the length of the estrous cycle when administered at 100 IU/d or greater. In this study, cows received 20 IU at each milking twice daily, and no apparent detrimental effects were observed (Table 4). No unfavorable reactions were noted to the twice daily injections. Several cows exhibited increased anxiety during udder preparation early in the study; however, cows adjusted within a few weeks. No abscesses were detected at the site of injections. CONCLUSIONS
Administration of exogenous oxytocin to cows for a full lactation increased milk yield by 11.6% over cows not receiving oxytocin, but no alteration in milk composition or apparent difference in reproductive or health parameters occurred. It appears that most of the increase in milk yield occurred during the declining phase of lactation. Possible mechanisms for this action were proposed, but future research is needed to understand these mechanisms and the importance of timing of machine attachment relative to initiation of udder preparation. Mastitis appeared to negate the effect of oxytocin administration. Warning
The use of exogenous oxytocin in herds for milk production reasons is presently prohibited
by the United States Food and Drug Administration; thus, its use as a management tool is illegal and not recommended. REFERENCES 1 Adams. H. P., and N. N. Allen. 1952. The value of oxytocin for reducing fluctuations in milk and fat yield. J. Dairy Sci. 35:1117. 2 Adams, H. P., and N. N. Allen. 1952. The effect of removal of residual milk by use of oxytocin upon the yield and fat content of subsequent milkings. J. Dairy Sci. 35:1121. 3 Armstrong. D. T.• and W. Hansel. 1959. Alteration of the bovine estrous cycle with oxytocin. J. Dairy Sci. 42:533. Journal of Dairy Science Vol. 74, No.7, 1991
4Benson, G. K., and S. J. Folley. 1957. The effect of oxytocin on mammary gland involution in the mt. J. Endocrinol. 16:189. 5 Brandsma, S. 1978. The relation between milking. residual milk and milk yield. Page 47 in Proc. Int. Symp. Machine Milking, Louisville, KY, Natl. Mastitis COUIlC., Washington, DC. 6 CaruoIo, E. V. 1971. Exogenous oxytocin and lactation in the mouse. J. Dairy Sci. 54:1207. 7 DcPeters, E. J., N. E. Smith, and J. Acedo-Rico. 1985. Three or two times daily milking of older cows and first lactation cows for entire lactations. J. Dairy Sci. 68:123. 8 Donker, J. D., J. H. Koshi, and W. E. Petersen. 1954. The effects of hourly milking with the aid of intravenous injection of oxytocin. J. Dairy Sci. 37:1261. 9 Ely, F., and W. E. Petersen. 1941. Factors involved in the ejection of milk. J. Dairy Sci. 24:211. 10 Gavin, W. 1913. On the effects of administration of extracts of pituitary body and corpus luteum to milch cows. Q. J. Exp. Physiol. 6:13. 11 Gorewit, R C., and R Sagi. 1984. Effects of exogenous oxytocin on production and milking variables of cows. J. Dairy Sci. 67:2050. 12 Graf, G. C. 1968. Effects of oxytocin injected intramuscularly and intravenously on milk ejection of bovine. J. Dairy Sci. 51(SuppI. 1):628.(Abstr.) 13 Hansel, W., and W. C. Wagner. 1960. Luteal inhibition in the bovine as a result of oxytocin injections, uterine dilatation, and intrauterine infusions of seminal and preputial fluids. J. Dairy Sci. 43:796. 14 Henderson, A. J., and M. Peaker. 1984. Feed-back control of milk secretion in the goat by a chemical in milk. J. Physiol. 351:39. 15 Hill, R. L., and S. Simpson. 1914. The effect of pituitary extract on the secretion of milk in the cow. Proc. Soc. Exp. BioI. Med. 11:82. 16 Knodt, C. B., and W. E. Petersen. 1942. The effect of the continuous injection of pitocin upon milk and milk fat production. J. Dairy Sci. 25:709. 17Knodl, C. B., and W. E. Petersen. 1944. The effect of complete evacuation of the mammary gland by pitocin upon milk and fat production. J. Dairy Sci. 27:449. 18 Koshi, J. H.• and W. E. Petersen. 1955. Complementary milk and its relationship to lactation. J. Dairy Sci. 38:788. 19 Merrill, W. G., R. Sagi, L. G. Petersson, T. V. Bui, H. N. Erb, D. M. Galton, and R. Gates. 1987. Effects of premilking stimulation on complete lactation milk yield and milking performance. J. Dairy Sci. 70:1676. 20 National Mastitis Council. 1981. Microbiological procedures for usc in the diagnosis of bovine mastitis. Natl. Mastitis Counc., Washington, DC. 21 Petersen, W. E., and T. V. Rigor. 1932. Relation of pressure to mte and quality of milk secreted. Proc. Soc. Exp. BioI. MOO. 30:254. 22 Premachandra, B. N., G. W. Pipes, and R. von Bersvordt-Wallmbe. 1959. Comparison of the intravenous and subcutaneous injections of oxytocin in the lactating cow. J. Dairy Sci. 42:918. 23 Sagi, R., R. C. Gorewil, and D. B. Wilson. 1980. Role of exogeDOns oxytocin in eliciting milk ejection in dairy cows. J. Dairy Sci. 63:2006.
EXOGENOUS OXYTOCIN AND MILK PERFORMANCE
24 SAS® User's Guide: Statistics, Version 5 Edition. 1985. SAS Inst, Inc., Cary, NC. 25 Shaw, J. C. 1942. The effect of oxytocin on milk and milk fat secretion. 1. Dairy Sci. 25:1051. 26 Smith, V. R. 1947. The effect of milking at short intervals with and without injections of oxytocin. 1. Dairy Sci. 30:703. 27 Sprain, D. G., V. R. Smith, W. 1. Tyler, and O. T. Fosgate. 1954. The effect on milk and fat production of injections of oxytocin at alternate 14-day periods during lactation. 1. Dairy Sci. 37:195. 28 Thatcher, W. W., and H. A. Tucker. 1970. Lactational performance of rats injected with oxytocin, cortisol21-acetate, prolactin, and growth hormone during prolonged lactation. Endocrinology 86:237. 29 Thompson, P. D., M. 1. Paape, and J. W. Smith. 1973.
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Residual milk yield as affected by dose and time of injection of oxytocin. J. Dairy Res. 40:221. 30 Tucker, H. A., R. P. Reece, and R. E. Mather. 1961. Udder capacity estimates as affected by rate of milk secretion and intramammary pressure. J. Dairy Sci. 44:1725. 31 Wachs, E. A., R C. Gorewit, and W. B. Currie. 1984. Oxytocin concentration of cattle in response to milking stimuli through lactation and mammary involution. Domest. Anim. Endocrinol. 1:141. 32 Wood, P.D.P. 1967. Algebraic model of the lactation curve in cattle. Nature (Lond.) 216:164. 33 Wildman, E. E., G. M. lones, P. E. Wagner, and R. L. Boman. 1982. A dairy cow body condition scoring system and its relationship to selected production characteristics. J. Dairy Sci. 65:495.
Journal of Dairy Science Vol. 74, No.7, 1991