Estrogen in plasma of parturient paretic and normal cows

The endocrine factors associated with parturient paresis have not been defined totally. Estrogens stimulate uptake of calcium by bone. Since secretion of estrogen increases dramatically as parturition approaches, estrogen may be involved in homeostatic mechanisms regulating calcium metabolism. Plasm...

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Published inJournal of dairy science Vol. 62; no. 4; pp. 551 - 556
Main Authors Sasser, R.G, Falk, D.E, Ross, R.H
Format Journal Article
LanguageEnglish
Published United States Am Dairy Sci Assoc 01.04.1979
American Dairy Science Association
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Summary:The endocrine factors associated with parturient paresis have not been defined totally. Estrogens stimulate uptake of calcium by bone. Since secretion of estrogen increases dramatically as parturition approaches, estrogen may be involved in homeostatic mechanisms regulating calcium metabolism. Plasma was collected for 30 days (-30) prepartum to 5 days (+5) postpartum from six Holstein and nine Jersey cows approaching three or more lactations. Of all cows, six Jerseys contracted parturient paresis. Estradiol and estrone were analyzed by radioimmunoassay, total calcium and total magnesium by atomic absorption spectrophotometry, and total phosphorus by colorimetry. Data were grouped into periods respresenting days -30 to -21, -20 to -11, -10 to -6, -5 to -4, -3 to -2, -1, 0 (parturition), +1, +2 to +3, and +4 to +5. Calcium in plasma was lower in parturient paresis cows on days +1 and +2 to +3, and magnesium was higher during the same periods but lower on days -4 to -5. Total phosphorus, estrone, and estradiol of normal cows and those with parturient paresis were not different. During the entire sampling period, phosphorus and estradiol were similar in both groups while magnesium was higher and calcium lower in cows with parturient paresis. Estrone was lower in cows with parturient paresis. Lower estrone in cows with parturient paresis may be predisposing for parturient paresis.
Bibliography:L10
7912729
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ISSN:0022-0302
1525-3198
DOI:10.3168/jds.S0022-0302(79)83289-0