Endocrine changes in sows exposed to elevated ambient temperature during lactation

DOMESTICANIMALENDOCRINOLOGY

Vol. 8(1):117-127,1991

ENDOCRINE CHANGES IN SOWS EXPOSED TO ELEVATED AMBIENT TEMPERATURE DURING LACTATION C.R. Barb .1, M.J. Estienne *.2, R.R. Kraeling*, D.N. Marple***, G.B. Rampacek**, C.H. Rahe***, J.L. Sartin*** *U.S. Department of Agriculture Athens, GA 30613, **University of Georgia, Athens, GA 30602 and ***Auburn University, Auburn AL 36830 Received May 11, 1990

ABSTRACT Seven sows were placed into one of two environmental chambers at 22 C, 5 d prior to farrowing. On day 9 of lactation, one chamber was changed to 30 C (n=4) and the other remained at 22 C (n=3). On days 24 and 25, blood samples were collected every 15 min for 9 hr and 7 hr, respectively. On day 24, thyrotropin releasing hormone (TRH) and gonadotropin releasing hormone (GnRI-t) were injected iv at hour 8. On day 25 naloxone (NAL) was administered iv at hour 4 followed 2 hr later by iv injection of TRH and GnRH. Milk yield and litter weights were similar but backfat thickness (BF) was greater in 22 C sows (P<.05) compared to 30 C sows. Luteinizing hormone (LH) pulse frequency was greater (P<.003) and LH pulse amplitude was less (P<.03) in 22 C sows. LH concentrations after GnRH were similar on day 24 but on day 25, LH concentrations after GnRH were greater (P<.05) for 30 C sows. Prolactin (PRL) concentrations were similar on days 24 and 25 for both groups. However, PRL response to TRH was greater (P<.05) on both days 24 and 25 in 30 C sows. Growth hormone (GH) concentrations, and the GH response to TRH, were greater (P<.0001) in 30 C sows. Cortisol concentrations, and the response to NAL, were less (P<.03) in 30 C sows. NAL failed to alter LH secretion but decreased (P<.05) PRL secretion in both groups of sows. However, GH response to NAL was greater (P<.05) in 30 C sows. Therefore, sows exposed to elevated ambient temperature during lactation exhibited altered endocrine function.

INTRODUCTION Reports on the effect of temperature on secretion of hormones which affect reproduction and lactation in the pig are extremely limited. Wettemann and Bazer (1) reported that plasma prolactin (PRL) concentrations were increased in gilts exposed to 32 C during days 8-16 after mating, compared with concentrations in pregnant and unmated gilts exposed to 21 C. Kraeling et al. (2) demonstrated that PRL release after thyrotropin releasing hormone (TRH) was greater in gilts exposed to 30 C than gilts exposed to 20 C suggesting a temperature-related change in pituitary responsiveness. Recently, Flowers and Day (3) reported that the post-castration increase in LH secretion was suppressed in prepuberal gilts exposed to elevated ambient temperature. Recent work by this laboratory has demonstrated that treatment of lactating sows with naloxone (NAL), an e n d o g e n o u s opioid peptide (EOP) antagonist, resulted in a significant increase in serum luteinizing hormone (LH) concentrations (4) and a decrease in PRL release (5). This study was conducted during November when the ambient temperature averaged 20 C in the farrowing house. However, in an earlier study (Barb, unpublished) conducted in the lactating sow during June, when the ambient temperature averaged 32 C in the farrowing house, NAL treatCopyright © 1991 by Domendo, Inc.

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ment failed to alter LH secretion. Thus, we hypothesized that temperature" ma? influence EOP m o d u l a t i o n of anterior pituitary h o r m o n e secretion. Normally, gonadotropin secretion increases gradually during late lactation in sows and more dramatically following weaning (6,7) culminating in estrus within 4 to 10 d al~ter weaning (8,9). Typically, intervals from weaning to estrus are longer in late sun> mer or early fall than during other seasons and this delay is greater in primiparous than multiparous sows (10,11). The present experiment was conducted to compare feed intake, body condition and endocrine function in primiparous sows exposed to elevated ambient temperature during lactation. MATERIALS AND METHODS T w o to 5 d prior to farrowing, 7 primiparous sows, (139.9 + 5.2 kg b o d y weight, BW) were each randomly placed into two identical environmental chambers set at 22 C and 13 hr light: 11 hr dark. On day 9 of lactation (d 0=day of farrowing) one chamber was changed to 30 C (n=4) and the other remained at 22 C (n=3). There was no difference in the n u m b e r of pigs suckled and averaged 8.9 -+ 0.3 pigs across groups. Backfat thickness (BF) was assessed on days 9 and 24 of lactation using ultrasound. Milk yield was determined on day 21 by the weighsuckle-weigh procedure (12). During lactation, sows were fed free choice, a cornsoybean meal diet s u p p l e m e n t e d with vitamins and minerals according to NRC (1983) guidelines. A cannula was placed non-surgically into the jugular vein (13) of all sows on day 23. On days 24 and 25, blood samples were collected every 15 min for 9 hr and 7 hr, respectively. At hour 8 on day 24, .5 g/kg BW of TRH and gonadotropin releasing h o r m o n e (GnRH) were injected h,. On day 25, at hour 4, 1 mg NAL3/kg BW was administered iv followed 2 hr later by iv injection of TRH and GnRH at the same doses given above. H o r m o n e Assays. Luteinizing h o r m o n e and PRL were quantified in all samples by double antibody radioimmunoassays (RIA) described previously by Kraeling et al. (14). The intra- and inter-assay coefficients of variation for LH were 8.4 and 10.5% and for PRL were 16.3 and 15.2%, respectively. Cortisol was quantified in hourly samples by a RIA described by Fonda et al. (15) in which the intra- and inter-assay coefficients of variation were 3.2 and 9.5%, respectively. Serum progesterone was quantified by RIA (16) on the first sample collected on day 24. Intraassay coefficient of variation was 9.3%. Total serum thyroxine (T4) concentrations were quantified on the sample prior to and 1 hr after TRH by a RIA Kit ~'. A R I A previously described by Marple and Aberle (17) and modified for use in our laboratory was used to quantify GH in all samples. The primary antiserum AFP1031854, produced in monkeys against porcine GH, was kindly provided by Dr. A.F. Parlow, Harbor-UCLA Medical Center, Torrance, CA and used at 1:80,000 dilution. Rabbit anti-monkey g a m m a globulin 4 serum was used as a precipitating agent at a 1:20 dilution. Purified porcine GH was used for iodination (USDA-pGH-I-1) and standards (USDA-pGH-B-1). Dose response curves for pooled porcine serum and increasing concentrations of GH standard added to a porcine serum pool were parallel (P>.10) to the standard curve. The .08 to 5 ng of GH added to porcine serum was consistently recovered from 200 ~1 of serum (99 + 2%). Cross-reactions of the primary antiserum with large quantities (100 to 10,000 ng) of porcine PRL (AFP9764B), follicle stimulating h o r m o n e (AFP9440C), LH (AFP432B) and TRH (AFP5128B) were not detected. Sensitivity of the assay was .08 ng/tube, lntra- and inter-assay coefficients of variation were 3.2% and 13.6%, respectively.

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Statistical A n a l y s i s , Sampling time for LH, PRL, and GH was divided into two periods on day 24. Period 1 represented the m e a n of samples collected prior to GnRH/TRH treatment and Period 2 the samples collected after treatment. On day 25, sampling time was divided into four periods. Period 1 represented the mean of samples collected prior to NAL treatment. The remainder of the sampling time was divided into three consecutive 1 hr periods. Luteinizing hormone, PRL, GH, and cortisol data were subjected to a split plotin-time analysis of variance using the general linear m o d e l p r o c e d u r e of the Statistical Analysis System (18). Treatment, pig, and period were considered discrete (class) variables. The effect of treatment was tested using pig within treatment as the error term. The effect of period and the treatment x period interaction w e r e tested using pig within treatment x period. Differences b e t w e e n period means within and b e t w e e n treatment groups were determined by least-squares contrasts by the SAS procedure. A sow was classified as responding to NAL w h e n concentrations of LH at 30 rain after treatment were 50% greater than the pretreatment m e a n for LH (4). Within animals, basal and pulse characteristics for serum LH profiles were calculated by the procedure of Barb et al. (19). To evaluate the effect of temperature on basal serum LH concentrations, number of LH peaks and amplitude of LH peaks, data were subjected to analysis of variance using the general linear model procedure of SAS (18). Treatment, pig and day were discrete variables. The effect of treatment was tested using pig within treatment as the error term. The effect of day and the treatment x day interaction were tested using pig within t r e a t m e n t x day. Serum T4 concentrations, milk p r o d u c t i o n and litter weights on day 21, feed intake during the treatment period and change in BF from day 9 to day 24, were subjected to analysis of variance using the general linear model procedure of SAS, (18). RESULTS Milk yield on day 21 tended to be greater (P<.08) for sows maintained at 22 C than for sows at 30 C, while litter weights were similar (table 1). Sows exposed to 30 C consumed less (P<.002) feed and lost more BF (P<.05) than 22 C sows (table 2). Since there was no temperature x day interaction for the indices of LH secretion, data were pooled across days for the pretreatment (i.e., before TRH/GnRH on day 24 and before NAL on day 25) bleeding periods. Mean serum LH concentrations were not influended (P>.I) by temperature. However, LH pulse frequency decreased (P<.003) and LH pulse amplitude increased (P<.03) in sows maintained at 30 C c o m p a r e d to 22 C (table 3). Mean serum LH concentrations were similar on day 24 for the 22 C and 30 C sows prior to (.27 + .1 and .32 -+ .07 ng/ml, respectively) and after GnRH (1.5 + .3 and 1.9 + .3 ng/ml, respectively). However, the LH response to GnRH was greater (P<.001) in 30 C sows than 22 C sows on day 25 (figure 1). Mean serum PRL concentrations were similar for 30 C sows (25.3 + 9.1 ng/ml) and 22 C sows (24.7 + 10.5 ng/ml) on day 24. However, the PRL

TABLE. 1. MILK YIELD AND LITIXR WEIGHT ON DAY 21 oF LACTATIONFOR SOWS MAINTAINED AT 22 C AND 30 C ~

Treatment 22 C 30C a M e a n + SEM *(P<.08)

No. o f sows

Piglets per sow

Litter weil~ht ( k ~

Milk y i e l d (kg,/day)

3 4

8.7 - .3 9.2 + .4

52.1 _+ 1.9 50.1 + .4

6.7 + 1.0" 5.0 + .2

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TABLE 2. INFLUENCE OF TEMI'ERA'R RY FROM DAYS 9 TO 2~i OF I.ACIArI()N t) x, }2I El) [N'I,\KF AND }[)lII ]{ll; 1"~,\{ K! \ FO~ Sows M~,r, TAINED.,vr 22 C AXl) 30 C'

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0.1 1R,,i47

Matabolizable Energy Intake (kcal d a y ) Curde Protein ( g / d a y ) Decrease in Backfat ( r a m ) from Day 9

853 1.6

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r e s p o n s e to TRH w a s greater (P<.05) in 30 C s o w s (171 _+ 26 n g / m l ) than in 22 C s o w s (83 + 30 n g / m l ) . A similar effect o f t e m p e r a t u r e o n PRL s e c r e t i o n w a s o b s e r v e d o n day 25 (figure 2). M e a n s e r u m GH c o n c e n t r a t i o n s and the GH r e s p o n s e to TRH w e r e greater (P<.0001) in 30 C (3.8 + .1 ng/ml; 8.3 _+ .3 ng/ml, respectively) than in 22 C (2.7 + .1 ng/ml: 3.6 + .4 ng/ml, respectively) s o w s on day 24. A similar effect on GH secretion w a s o b s e r v e d on day 25 (figure 3). N a l o x o n e failed to alter LH secretion in the 22 C s o w s (figure 1 ). The increase in serum LH concentrations during the first hr after NAL in the 30 C s o w s w a s the restilt of o n e s o w w h i c h r e s p o n d e d to NAL treatment (Figure 1). Serum PRL c o n centrations d e c r e a s e d (P<.05) similarly in the 30 C and 22 C s o w s t o l l o w i n g NAL treatment (Figure 2). Serum GH concentrations d e c r e a s e d (P<.05) and w e r e nol different during the first hr after NAL in both groups of s o w s , but by the s e c o n d hr s e r u m GH c o n c e n t r a t i o n s w e r e less (P<.O02) in 22 C s o w s than in 30 C s o w s (Figure 3). Exposure of s o w s to 30 C s u p p r e s s e d (P<.03) serum cortisol concentrations and the cortisol r e s p o n s e to NAL c o m p a r e d to 22 C s o w s (Figure 4). Serum proges-

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PERIOD Fig. 1. Serum luteinizing h o r m o n e (Mean ± SE) on d a y 25 for s o w s maintained at either 22 C ()r 30 (i. Period 1 = prior to n a l o x o n e (NAL), P e r i o d 2 = first hr after NAL, Period 5 = s e c o n d hr after NAL, a n d Period 4 = first hr after GnRH. Bars with different superscripts differ (P<.O01).

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TABLE 3. MEAN SERUMLH CONCENTRATIONS, LH PEAKAMPLITUDE, LH PEAK FREQUENCYFOR SOWS MAINTAINED AT 22 C AND 30 C~

Treatment 22 C 30 C

No. of sows

Mean serum LH concentrations (ng/ml)

LH peak amplitude (ng/ml)

Frequency of LH pulses/h

3 4

.25 +- .02 .33 ± .03

.17 _+ .09* .55 ± .06

.46 ± .07** .24 _+ .02

~Mean +_ SEM, data pooled from days 24 and 25 for the pretreatment bleeding periods. Means in a column differ, *(P<.03), **(P<.003)

terone concentrations were below assay sensitivity (1 ng/ml) for both groups of sows. Concentrations of serum T~ were unchanged by temperature and averaged 6.6 + 1.4 ng/ml and 9.6 + 1.1 ng/ml for 30 C and 22 C sows, respectively. However, serum T~ concentrations increased (P<.02) after TRH administration in 22 C sows (12.5 + 1.1 ng/ml) but not in 30 C sows (6.8 _+ 1.0 ng/ml). DISCUSSION

Luteinizing hormone pulse frequency decreased dramatically in sows exposed to 30 C. Since pituitary responsiveness to exogenous GnRH was uncompromised by elevated ambient temperature, reduction in LH pulse frequency m a y reflect a decrease in hypothalamic discharge of GnRH. The increased LH pulse amplitude observed in the 30 C sows may reflect an increase in releasable pituitary LH and may in part explain the variability in the LH response to GnRH in the 30 C sows on days 24 and 25. Reports in the dairy cow (20) and ewe (21) demonstrated that heat stress lowered serum LH concentrations and suppressed the preovulatory LH surge, while a recent report by Wise et al. (22) illustrated that acute heat stress suppressed pulsatile secretion of LH in the dairy cow. Although the mechanism by

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Fig. 4. Serura cortisol c o n c e n t r a t i o n s ( M e a n _+ SE) on d a y 25 t"<>i"s o w s m a i n t a i n e d at 22 C or 30 C. P e r i o d 1 = prior to n a l o x o n e (NAL) a n d Period 2 = fi~ree hr s a m p l e s after NAL. Bars with diff~_'rent s u p e r s c r i p t s differ @<.03).

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which elevated ambient temperature disrupts function of the hypothalamic-pituitary axis cannot be ascertained by the current study, nutritional intake during lactation could be involved. Sows exposed to 30 C consumed less feed and subsequently metabolized more of their body reserves of adipose tissue than sows at 22 C. Energy restriction during lactation resulted in greater weight and BF loss in primiparous sows during lactation and prolonged the postpartum anestrous period (23,24,25). In addition, the interval from weaning to estrus was inversely related to changes in BW (26) and heartgirth (27,28). Several reports demonstrated that the postpartum interval was significantly greater for sows farrowing in spring and summer m o n t h s than for sows farrowing in fall and w i n t e r m o n t h s (29,30,31). Moreover, Armstrong et al. (32) reported that feed intake, backfat, hypothalamic GnRH content and concentration of LH in the serum and pituitary were lower in sows weaned in summer than those weaned in winter. In contrast, the effect of nutritional restriction independent of elevated temperature on LH secretion in the sow is equivocal. Armstrong et al (28) reported that energy restriction during lactation in primiparous sows failed to alter post-weaning reproductive performance and LH secretion, while protein restriction in first litter sows during lactation decreased mean LH concentrations but failed to alter LH pulse frequency and pulse amplitude (33). Therefore, the results of the present study provide evidence that the reduced fertility and prolonged duration of the post-weaning anestrous period in sows w e a n e d during the summer months may in part be the result of a decrease in LH pulse frequency caused by altered dietary intake induced by exposure to elevated ambient temperature. Depressed serum LH concentrations during heat stress have been attributed to inhibitory action of adrenal steroids on the hypothalamic-pituitary axis (34). It was postulated that heat stress results in release of adrenocorticotropic h o r m o n e (AGFH) and subsequent increase in adrenal secretion of progesterone and glucocorticoids. An ACTH dependent release of progesterone from the adrenal has been demonstrated in the pig (35). Results from the present study, however, demonstrate that temperature failed to influence serum progesterone concentrations. Similar results were observed in heat stressed prepuberal (36) and pregnant gilts (37). In addition, serum cortisol concentrations were less in sows exposed to 30 C than 22 C, as was the cortisol response to NAL. This is consistent with the observation that serum cortisol concentrations were lower during the summer months than during the remainder of the year in pregnant sows (38) and that basal and ACTHstimulated cortisol secretion were suppressed in ovariectomized sows exposed to elevated ambient temperatures (39). We previously demonstrated that increased serum cortisol secretion following NAL administration in the gilt is primarily due to action at the level of the CNS (40). These results coupled with our present findings and that of Seren et al. (39), suggest that the responsiveness of the hypothalamicpituitary-adrenal axis is suppressed by chronic exposure to elevated ambient temperature. Furthermore, cortisol secretion may also be affected by restricted nutritional intake. Therefore, reduction in cortisol secretion in sows maintained at 30 C contradicts the idea that elevated temperature alters reproductive process by increasing adrenal cortisol secretion. In support of this notion, Gindoff and Ferin (41) demonstrated that corticotropin-releasing factor (CRF) induced suppression of LH secretion in the primate is independent of glucocorticoid secretion. Although a seasonal influence on GH secretion has not been reported, an influence on PRL secretion has been reported for the pig, with highest serum PRL concentrations occurring during the summer months (42). Under the conditions of this

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experiment, increasing environmental temperature from 22 C to 30 C for 16 (t failed to alter basal PRL secretion but increased basal GH secretion, while both the PRL and GH response to TRH was enhanced. Similar findings regarding PRL secretion have been reported in ovariectomized gilts maintained at 30 C (2). Thus, the pig is unlike the cow and sheep in which both basal serum concentration of PRL a n d s e r u m PRL r e s p o n s e to TRH were i n c r e a s e d by i n c r e a s e d t e m p e r a t u r e (21,43,44). In addition, basal concentrations of GH and the GH response to TRH were unchanged by elevated temperature in the heifer (45). We believe that duration of treatment imposed in this study was sufficient to alter basal secretion of PRL. Tucker (46) demonstrated that PRL secretion in the heifer responded within a few days to temperature elevation, while in the gilt PRL concentrations were unchanged after exposure for 30 d to 30 C (2). It should be noted, that in the sheep and cattle studies cited above, there was no observable reduction in nutrient intake. Therefore, the physiological status of the sows in the present study and ruminants in the above studies are quite different. The significance of the temperature-induced alteration in serum PRL and GH response to TRH and basal GH secretion is not clear. The heatqnduced elevation of GH concentrations may be a manifestation of the altered metabolic state of the animal, since a variety of dietary and metabolic perturbations alter GH secretion (47,48,49). It is conceivable that temperature a n d / o r dietary perturbations may also influence factors modulating stores of PRL and GH in the anterior pituitary gland and thereby influence GH and PRL response to TRH. We and others previously demonstrated that EOP are involved in the sucklinginduced suppression of LH and stimulation of PRL secretion in the lactating sow (4,5,50,51) and recently we reported that the EOP are involved in modulating GH secretion in the gilt (52). G w o s d o w et al. (53) reported elevated plasma and pituitary beta-endorphin concentrations in rats exposed to 32.5 C. In the present study, NAL treatment was employed to determine if temperature influenced EOP modulation of pituitary h o r m o n e secretion. Unexpectedly, NAL, at a dose previously shown to increase LH concentrations in postpartum sows (4), failed to stimulate LH secretion in both groups of sows. The lack of an LH response to NAL may, in part, be due to one of the following: 1) the dose of NAL was insufficient to antagonize the EOP; 2) hypothalamic responsiveness to NAL and subsequent GnRH release was greater in sows of our previous study (4) compared to this study. Serum PRL concentrations decreased similarly in 22 C and 30 C sows alter NAL treatment which, is in agreement with previous work in the sow (5,50,51). In contrast, GH response to NAL was reduced in sows maintained at 30 C, suggesting that elevated temperature a n d / o r altered dietary intake could conceivably alter sensitivity of EOP pathways which modulate GH secretion. In support of this idea, Armario et al. (54) reported that chronic stress enhanced the GH response to the EOP agonist morphine in the rat. Moreover, several studies have demonstrated that perturbations in dietary intake can alter hypothalamic EOP content (55). In conclusion, the decrease in LH secretion and aberrations in the endocrine system observed in sows at 30 C c o m p a r e d to sows at 22 C, may in part be responsible for the longer weaning to estrus interval in sows weaned during the summer. However a concomitant reduction in feed intake during lactation may be involved in the aberrations of the endocrine system. ACKNOWLEDGEMENTS/FOOTNOTES The authors wish to thank Ms. Elizabeth A. Taras and Mr. Bennett Johnson for their technical assistance; Ruel L. Wilson, biometrician, Southern Region, ARS, ff)r his statistical advice; Dr. J. Bolt, USDA,

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Beltsville, MD, for providing pituitary hormones used in radioimmunoassay; and Dr. Myron Brown, Ceva Laboratory, Overland Park, KS, for the generous gift of GnRH. *Please address correspondence to: Dr. C. Richard Barb, Animal Physiology Research Unit, R.B. Russell Agricultural Research Center, P.O. Box 5677, Athens, GA 30613. 2Present address: Department of Agriculture, University of Maryland Eastern Shore, Princess Anne, MD 21853. ~Sigma Chemical Co., St. Louis, MO ~Cambridge Medical Corp., Billerica, MA Mention of a trade name, proprietary product, or specific equipment does not constitute a guarantee or warranty by the USDA and does not imply its approval to the exclusion of other products that may be suitable. REFERENCES 1. Wettemann RP, Bazer FW. Influence of environmental temperature on prolificacy of pigs. In: Foxcroff GR, Cole DJA, Weir BJ (eds.) Control of Pig Reproduction II, p 199208, 1988. 2. Kraeling RR, Marple DN, Rampacek GB, Rahe CH, Sartin JL. Effect of photoperiod and temperature on prolactin secretion in ovariectomized gilts. J Anim Sci 64:1690-1695, 1987. 3. Flowers B, Day BN. Alterations in gonadotropin secretion and ovarian function in prepubertal gilts by elevated environmental temperature. Biol Reprod 42:465-471, 1990. 4. Barb CR, Kraeling RR, Rampacek GB, Whisnant CS. Opioid inhibition of luteinizing hormone secretion in the postpartum lactating sow. Biol Reprod 35:368-371, 1987. 5. Barb CR, Kraeling RR, Rampacek GB, Leshin LS. Opioid modulation of follicle stimulating hormone (FSH) and prolactin (PRL) secretion in the postpartum sow. In: Mahesh VB (ed.) Regulation of ovarian and testicular function, Pleum Publishing Corp, New York, p. 647-652, 1987. 6. Stevenson JS, Britt JH. Interval to estrus in sows and performance of pigs following daily separation of sow and litter or altered litter size during late lactation. J Anim Sci 53:179-181, 1981. 7. Bevers MM, Willemse AH, Kruip Th AM, Van de Wiel DFM. Prolactin levels and the LH response to synthetic LH-RH in the lactating sow. Anim Reprod Sci 4:155-163, 1981. 8. Svagr AJ, Hays VW, Cromwell GL, Dutt RH. Effect of lactation duration on reproductive performance of sows. J Anita Sci 38:100-105, 1974. 9. Cole DJA, Varley MA, Hughes PE. Studies in sow reproduction. 2. The effect of lactation length on the subsequent reproductive performance of the sow. Anita Prod 20:401-406, 1975. 10. Britt JH, Armstrong JD, Cox NM, Esbenshade KL. Control of follicular development in the postpartum sow. J Reprod Fertil [Suppl] 33:37-54, 1985. 11. Claus R, Weiler W. Influence of light and photoperiodicity on pig prolificacy. J Reprod Fertil [Suppl] 33:185-197, 1985. 12. Lewis AJ, Speer VC, Haught DG. Relationship between yield and composition of sow's milk and weight gains of nursing pigs. J Anita Sci 47:634-638, 1978. 13. Barb CR, Kraeling RR, Rampacek GB, Fonda ES, Kiser TE. Inhibition of ovulation and LH secretion in the gilt after treatment with ACTH or hydrocortisone. J Reprod Fertil 64:85-92, 1982. 14. Kraeling RR, Rampacek GB, Cox NM, Kiser TE. Prolactin and luteinizing hormone secretion after bromocryptine (CB-154) treatment in lactating sows and ovariectomized gilts. J Anim Sci 54:1212-1220, 1982. 15. Fonda ES, Rampacek GB, Kraeling RR, Hart MA. Effect of storage time and temperature on steroid and p r o t e i n h o r m o n e c o n c e n t r a t i o n s in p o r c i n e p l a s m a and serum. Theriogenology 18:711-721, 1982. 16. Kraeling RR, Rampacek GB, Kiser TE. Corpus luteum function after indomethacin treatment during the estrous cycle and following hysterectomy in the gilt. Biol Reprod 25:511-518, 1981. 17. Marple DN, Aberle ED. Porcine plasma growth hormone levels: Radioimmunoassay techniques and its application. J Anita Sci 34:261-265, 1972. 18. SAS. SAS User's Guide: Statistics. SAS Inst. Inc., Cary, NC, 1985. 19. Barb CR, Rampacek GB, Kraeling RR, Estienne MJ, Taras E, Estienne CE, Whisnant CS. Absence of brain opioid peptide modulation of luteinizing hormone secretion in the prepubertal gilt. Biol Reprod 39:603-609, 1988. 20. Madan ML, Johnson HD. Environmental heat effects on bovine luteinizing hormone. J

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