P A R T U R I E N T P A R E S I S . IV. T H E E F F E C T OF U D D E R I N F L A T I O N U P O N B L O O D L E V E L S O F CALCIUM, M A G N E S I U M AND P H O S P H O R U S IN COWS W I T H P A R T U R I E N T P A R E S I S 1~2 R. P. N I E D E R I ~ E I E R AND Y E A R L R. S M I T H
Department of Dairy Husbandry, University of Wisconsin
Air inflation of the u d d e r was used extensively as a t r e a t m e n t for p a r t u r i e n t paresis until the development of calcium therapy. Even today, air inflation is resorted to in cases that do not respond to calcium t h e r a p y (23). Seitter (25) reported that inflation of the udders of anesthesized goats and cows produced a marked increase in blood pressure. Later A u g e r (4), using a more refined technique, concluded that air inflation caused only a slight increase in blood pressure. Maguire (20), W i d m a r k and Carlens (28) and Auger (3) report a marked increase of blood sugar a f t e r inflation of the u d d e r with air. Fish (10, 11), Sjollema (26) and H a y d e n (17) demonstrated that the hyperglycemia occurring after u d d e r inflation resulted from lactose in the blood, presumably absorbed from the m a m m a r y gland. Several workers have shown an increase in blood serum calcium following m a m m a r y inflation for milk fever treatment (9, 16, 27). Fish (12) demonstrated an increase in both serum calcium and inorganic phosphates. The mechanism whereby u d d e r inflation produces the above effects has been a source of much conjecture. Peterson and Rigor (19) and Garrison and T u r n e r (12) have reported that milk secretion is practically inhibited when air pressures of 25 to 40 ram. H g are maintained in the cow's udder. Some (9, 19) attribute the effect of inflation to the cessation of milk secretion, thereby preventing the further uptake of milk precursors from the blood. Others (6, 15) postulate that u d d e r inflation gives rise to afferent stimuli which are responsible for the curative effects. This work was u n d e r t a k e n to obtain, in more detail, the changes in calcium, magnesium and inorganic phosphorus during recovery from p a r t u r i e n t paresis a f t e r udder inflation. At the time the work was initiated, no one had reported studies on magnesium levels after inflation. In a recent study of p a r t u r i e n t paresis treated by air inflation, Robertson (23, 24) included data on magnesium levels. EXPERIMENTAL PROCEDURE
The udders of seven J e r s e y cows with p a r t u r i e n t paresis were inflated with air to a pressure of 60 to 70 ram. H g and the teats taped to prevent the escape of air. The pressure was measured with an aneroid manometer attached to a teat Received for publication Aug. 31, 1949. 1 P a r t of these data were taken from a thesis presented by R. P. Niedermeier to the graduate faculty of the University of Wisconsin in partial fulfillment of the requirements for the degree of Doctor of Philosophy. Published with approval of the Director of the Wisconsin Agricultural Experiment Station. 38
TABLE 1
Theeffectofudderinflationonealcium, pho~horusand magnesium ofcowswithpartu~entparesis Cow no. Time
12 Ca
P
20 Mg
Ca
P
63 Mg
Ca
P
494 Mg
P
705
732
Mg
Ca
P
Mg
Ca
P
Mg
Ca
P
~VIg
Preinflation 2.8 1.2
2.6
4.4
0.8
2.8
3.1
0.62
3.5
4.5
1.4
4.1
Postinflation 3.4 3.8 4.0 5.3 5.7 a 5.2 5.1 5.0 5.0
2.8 2.6 2.6 2.8 3.1 3.2 2.9 2.8 2.9
5.1 5.4 4.8a 4.9 5.0 5.4 6.0 6.1 6.8
0.7 0.9 1.0 0.8 1.4 3.7 3.5 3.2 2.8
2.8 2.8 3.0 3.1 3.2 3.5 3.2 3.3 3.6
3.7 4.3 4.1 4.3 4.7 a 4.8 4.6 4.6 4.0
0.87 1.09 1.06 1.23 1.15 0.87 1.62 2.13 1.70
3.7 3.8 3.7 3.7 3.7 3.6 3.8 3.8 3.9
5.1 5.6 5.4 6.0a 6.8 7.5 7.4 7.3 7.5 9.8 9.8
2.2 2.7 2.9 2.9 2.7 2.1 3.3 4.1 4.4 3.6 3.8
3.9 4.0 3.7 3.6 3.4 3.6 3.5 3.3 2.9 2.3 2.0
(rag. %)
-(h~..)
0.5 1.5 3.0 5.0 8.0 11.0 14.0 17.0 20.0 36.0 48.0
Ca
556
4.6
1.3
2.0
5.2
0.5
3.3
4.6
1.4
4.5
4.8 4.7 5.4 5.9 6.0 6.7 7.1a 8.2 8.5
2.1 1.5 1.7 2.7 3.3 3.8 4.7 6.0 6.4
1.9 2.2 2.2 2.3 2.4 2.7 2.4 2.6 2.6
5.0 5.1 5.1 6.0 6.9a 7.3 7.6 7.7 7.6
0.5 0.7 0.7 1.0 1.2 1.4 1.8 1.9 2.8
3.1 3.3 3.5 3.4 3.5 3.5 3.5 3.0 3.2
5.1 6.1 6.6 a 6.3 6.6 6.5 6.8 6.9 7.1 6.1 8.6
1.5 2.3 2.5 2.6 2.9 3.0 3.0 2.1 3.3 6.0 6.3
4.6 4.6 4.7 4.5 4.3 4.3 4.3 4.3 3.9 3.5 2.6
a Time a f t e r inflation when cow was f o u n d standing.
2.1 3.0 2.2 2.5 3.3 3.6 2.8 1.6 1.8
40
E. P. NEIDER1V~EIER AND VEARL R. SMITH
cannula. The cows were not t r e a t e d u n t i l t h e y were down a n d u n a b l e to rise. A sample of venous blood was d r a w n before inflation. Post-inflation samples were d r a w n at 0.5, 1.5, 3, 5, 8, 11, 14, 17, 20, 36 a n d 48 hr. Samples were analyzed for serum calcium, serum m a g n e s i u m a n d i n o r g a n i c phosphorus, a n d all analyses were made in d u p l i c a t e . Blood serum calcium was d e t e r m i n e d by the method of C l a r k a n d Co]lip (7), serum m a g n e s i u m a c c o r d i n g to Simonsen et al. (26) a n d p l a s m a i n o r g a n i c p h o s p h o r u s b y the F i s k e a n d S u b b a r o w m e t h o d (13). RESULTS AND DISCUSSION Table 1 shows the results of analyses of blood samples for t o t a l serum calcium, serum m a g n e s i u m a n d p l a s m a i n o r g a n i c phosphorus. Cow 494 was in a coma at the time of inflation. Cows 20 a n d 494 were r e i n f l a t e d 3 hr. a f t e r the first inflation as a p r e c a u t i o n a r y measure, b u t no relapses occurred. The time r e l a t i o n s h i p s f o r calving, occurrence of milk fever, t r e a t m e n t a n d recovery are shown in table 2. Recovery was r e g a r d e d as the time the cow arose to her feet a n d stood u p of TABLE 2 Summary of time of treatment and recovery in relation to calving
Parturient paresis Cow no.
Inflation completed
Times
Recovery
Times
Times
Hr.
Min.
Hr.
Min.
Hr.
Min.
6 7 39 17 15
oo 40 oo 40 30
7 9 46 19 17
40 oo 10 55 oo
9 17 49 27 20
40 oo 10 55 oo
705b
ii
45
14
30
19
30
732
22
00
28
10
33
10
12 20 63 494 556
a Measured from end of calving. b Suffered relapse 38 hr. after calving and was treated with an intravenous injection of calcium glueonate. A second injection of calcium gluconate was made 76 hr. after calving and the cow died suddenly, after apparent recovery 9 hr. after the second injection. h e r own accord. Time of r e c o v e r y r a n g e d from 3 to 14 hr. a f t e r t r e a t m e n t b y u d d e r inflation. The s e v e r i t y of the m i l k fever cases is reflected in the low t o t a l serum calcium a n d p h o s p h o r u s in all pre-inflation samples. I n o r g a n i c p h o s p h o r u s values as low as 0.5 mg. p e r cent also were r e p o r t e d by A l l c r o f t (2) f o r milk fever cows. W i t h the exception of cows 556 a n d 705, r e c o v e r y was noted when the calcium level was n e a r or above 6 mg. p e r cent. Cow 494 r e m a i n e d on h e r feet with a serum calcium level of only 5 rag. p e r cent at 20 hr. a f t e r inflation. I n the seven cases studied, p l a s m a p h o s p h o r u s levels increased following u d d e r inflation, b u t in no case could the p h o s p h o r u s level be considered w i t h i n the n o r m a l r a n g e when the cows got up. Blood s e r u m m a g n e s i u m levels r e m a i n e d in the n o r m a l to high n o r m a l range as r e p o r t e d by A l l c r o f t (2) in all cows except 63 a n d 732, where a h y p e r m a g n e s e m i a condition existed. R e c o v e r y was u n e v e n t f u l in all cows except 705. I n 705 the c a l c i u m a n d p h o s p h o r u s d i d not r e t u r n to n o r m a l up to 20 hr. a f t e r inflation. S h o r t l y a f t e r 20 hr. post-inflation, she h a d a relapse a n d
PARTURIENT PARESIS I V
41
was treated with calcium gluconate. Two days after the first attack 705 died suddenly after apparent recovery. Robertson (23) found no correlation upon statistical analysis of his data on 19 milk fever cases between blood magnesium levels and the symptomatology classification as proposed by Barker (5). Pribyl (22) suggested the symptoms of milk fever may be due to a magnesium narcosis. ~Hibbs et al. (18) reported that" upon intravenous injection of magnesium sulphate into cows, general anesthesia resulted when the serum magnesium reached a level of 7.5 rag. per cent. When the serum calcium then was raised to 17.5 mg. per cent by an injection of calcium gluconate, the cows regained consciousness, even though the serum magnesium remained at the same high level. They suggested that the relationship between serum calcium and serum magnesium may be of great importance in the symptomatology of milk fever. Allcroft (1) found that anesthesia was produced in goats when the serum magnesium was between 13.5 and 14.5 mg. per cent, with the serum calcium around 7 mg. per cent. He further comments (2) on the importance of the calcium and magnesium ratio, as well as t h e calcium phosphorus ratio in milk fever. These data show that there is a considerable difference between cows as to the blood levels of calcium, phosphorus and magnesium at the time of recovery. This suggests that possibly the relative levels of the calcium, magnesium and phosphorus are more important in the symptomatology of milk fever than the actual blood level of any one constituent. SUMMARY
Data are given for the blood levels of calcium, magnesium and phosphorus during the recovery period for seven cases of parturient paresis in Jersey cows which were treated by udder inflation. ACKNOWLEDGMENTS
The authors wish to express their appreciation to J. G. Adams, president of Biltmore Company, for making facilities and cows available at Biltmore Farms for part of this study. Also, the authors are especially grateful to Ted Besh, herd manager, and A. B. Christian, in charge of the health of the herd, of Biltmore Farms for their keen interest and full cooperation in the execution of the study. REFERENCES (1) ALLCRO~T, W . M . The Fate of Calcium and Magnesium in the Blood Stream of the Ruminant. Vet. J., 103: 157-176. 1947. (2) ALLCROFT, W . M . Observations on Some Metabolic Disorders of Cows as Evidenced by Chemical Analysis of Samples of Blood from Clinical Cases. (2) Some Aspects of Blood Chemistry. Vet. J., 103: 30-47. 1947. (3) AUGER, M . L . Reeherches sur la pathogenic de la fievre vitulaire. Rec. g~n. reed. vet., 35: 353-384. 1926. (4) AUGER, M. L. Recherches sur . . . fi6vre vitulaire . . . et le syndrome hypoglyc~mique .... , Monograph, 1926. (Quoted by Dryerre and Greig (9) (5) BARKER, J . R . Blood Plasma Changes and Variations in the Female Bovine Toxemias. Vet. Record, 51: 575-580. 1939.
42
E.P.
NEIDER~iEIER AND VEARL R. SMITH
(6) BOnnIE, G. F. Metabolic Disturbances in Ruminants. Vet. Record, 61: 85-86. 1949. (7) CLARK, E. P. AND COLLIP, J . B . A Study of the Tisdall Method for t h e D e t e r m i n a t i o n of Blood Serum Calcium with Suggested Modifications. J. Biol. Chem., 63: 461-464. 1925. (8) DRYERRE, It. AND GREIG, J . R . Milk Fever: ICs Possible Association with Derangements in I n t e r n a l Secretions. Vet. Record, 5: 225-231. 1925. (9) DRYERRE, H. AND GREIG, J . R . F~rther Studies in the Etiology of Milk Fever. Dumfries and Galloway Vet. Med. Assoc. Oliver and Boyd, London. 1928. (10) FISH, P . A . The Physiology of Milk Fever. I. Cornell Vet., 17: 99-120. 1927. (11) FISH, P . h . The Physiology of Milk Fever. II. J. Am. Vet. Med. Assoc., 78: 10-37. 1928. (12) FISH, P . A . Milk Fever. l l t h Intern. Vet. Cong., 3: 330-347. 1930. (13) F]SKE, C. H. AN]) SURBAaOW, Y. The Colorimetric Determination of Phosphorus. J . Biol. Chem., 66: 375-400. 1925. (14) GARRISON,E. R. AND TURNER, C . W . The Effect of Udder I r r i g a t i o n and Milking Interval on Milk Secretion. Mo. Agr. Expt. Sta. Research Bull. 234. 1936. (15) GRIEG,J . R . Milk Fever. ~'et. Record, 6: 625-633. 1926. (16) GRIEG, J . R . The Nature of Milk Fever. l l t h Intern. Vet. Cong., 3: 306-324. 1930. (17) I['IAYDEN, C . E . The Blood Sugar of the Cow in Milk Fever. Cornel] Yet., 17: 121-131. 1927. (18) HIBBS, J. W., KRAUSS, W. E., POUNDEN, W. D., MONROE, C. F., AND SUTTON, T. S. Studies on Milk Fever in Dairy Cows. I I . The Effect of V i t a m i n D on Some of the Blood Changes in Normal and Milk Fever Cows at Parturition. J. Dairy Sci., 29: 767-781. 1946. (19) LITTLE, W. L. AND WRmH% N. C. A Review of Some M o d e r n Theories of Milk Fever. Vet. J., 82: 185-191. 1926. (20) MAGUIRE, L . C . Etiology of Milk Fever. Vet. Record, 6. 52-53. 1926. (21) PETERSEN, W. E. AND RIGOR, F . V . Relation of Pressure to Rate and Quality of Milk Secreted. Proc. Soc. Expt. Biol. Med., SO: 254-256. 1932. (22) PRIBYL, E. Obsah elektrolytic v krevnim seru ov~e a koz a v krevfiim seru krav, p~i nSkterych chorobach, zymena chorobach v dobg gravidity a, puerperia. Zverol. Rozpravy Suppl. Zverol. Obzor., 7: 61-70; 73-78. 1933. (Nutr. Abstr. and Rev., 4: 88. 1934-35.) (23) ROBERTS0N, A. Some Observations on Milk Fever. Vet. Record, 61: 333-339. 1949. (2~) ROBERTSON, A., BURGESS, J. W., MARR, A., AND MILI~IE, J . C . Some Observations on Milk Fever. Vet. Record, 60. 505-508. 1948. (25) SEITTER, M. Experimentelle Untersuchungen fiber die physiologische Werkung der Luftensufllation in das E u t e r von K~ihen und Ziegen als Beitrag zur Aetiologie der Gebarparese des Rindes. Inaug. Dissertation, Stuttgart, 1910. (Quoted by Fish (11)). (26) SI~0NSEN, D. G., WESTOVER, L. M., AND WERe:MAN, M. The Determination of Serum Magnesium by the Molybdlvanadate Method for Phosphate. J. Biol. Chem., 169: 39-47. 1947. (27) SJOLT.]~MA, B. t~ber die Bedauting der Elektrolytkonstellation fiir den Organismus. Die Biochemie der Geb~rparese yon Kfihen. Biochem. Z., ~(} : 300-308. 1928. (28) WIDI~ARK, E. M. AI~D CARLENS, O. Durch Luftinblasen in das Euter milchgebender Tiere hervorgerufene Hyperglyki~mie. Biochem. Z., 158: 3-10. 1925.