Intrauterine and subcutaneous sites for estradiol benzoate (EB) injection were compared in 30 gilts to test their relative effectiveness for estrogen-induced maintenance of corpora lutea. Vehicle or EB was injected on d 10 through 14 of the estrous cycle and corpora lutea that were maintained through d 24 were regressed subsequently by exogenous prostaglandin F2 alpha (10 mg). Cycle length (days) was not altered in either subcutaneous (18.6 +/- .5) or intrauterine (19.8 +/- .8) control groups. Gilts receiving 10 mg EB/d sc had longer (P less than .05) cycles (28.6 +/- 2 d) than gilts treated with 100 micrograms EB at either the sc (24.2 +/- 1 d) or intrauterine sites (23.3 +/- 1.3 d). The latter two cycle lengths were longer (P less than .05) than control cycles, but not different from each other. Before d 24, progesterone concentrations (ng/ml serum) were greater (P less than .01) in EB-treated gilts (25.1 +/- 2.0) than in controls (13.0 +/- 2.7). Progesterone concentration patterns were similar between gilts treated at intrauterine or sc sites. Thus, EB-induced maintenance of corpora lutea was not enhanced by direct injection into the uterine lumen.

Two experiments were conducted to evaluate whether administration of recombinant porcine somatotropin (pST) to sows (Hampshire-Yorkshire) enhanced lactational performance. In Exp. 1, sows (n = 84) were fed a corn-soybean meal diet (17.8% CP), or a similar diet with 8% added fat, from d 108 of gestation to d 28 of lactation. Half of the sows fed each diet were injected with 6 mg/d of pST from d 108 of gestation to d 24 of lactation. Diets were fed at 2.27 kg/d from d 108 of gestation until farrowing and then were self-fed during lactation. By d 3 of lactation, litter size was standardized at 8 to 10 pigs per litter. Treating sows with pST resulted in a 10-fold increase (P less than .001) in serum somatotropin at 4 h postinjection. Serum glucose was increased (P less than .01) and serum triglycerides, creatinine, and urea N were decreased (P less than .01) by pST. During the summer, apparent heat stress occurred in pST-treated sows, resulting in 14 deaths. Most (10) of the deaths occurred just before, during, or shortly after farrowing. Fewer (P less than .08) deaths occurred when pST-treated sows were fed the diet with added fat. Sows treated with pST consumed less feed (P less than .10) and lost more backfat (P less than .10) during lactation than controls. Increasing the dietary fat did not prevent these changes. Weaning weights of pigs and milk yield of sows (estimated by deuterium oxide dilution) were not affected by pST treatment. In Exp. 2, sows (n = 42) were injected weekly with 0 or 70 mg of pST on d 3, 10, 17, and 24 of lactation. Litters were standardized by d 3 at 8 to 10 pigs, and sows were fed the same control (low fat) diet as in Exp. 1. Sows treated with pST consumed less feed and lost more weight and backfat during lactation than untreated sows. Litter size, average pig weaning weights, and milk yield were not influenced by pST treatment. These data indicate that a 6-mg daily injection of pST from 6 d prepartum to d 24 of lactation or a 70-mg weekly injection of pST from 3 d postpartum to d 24 of lactation does not increase milk production in lactating sows.

Experiments were conducted to determine the role of estrogens on endogenous PGF2 alpha secretion and luteolysis following injection of cloprostenol in heifers. In Exp. 1, eight luteal-phase heifers were used to evaluate tamoxifen (T) as an estrogen antagonist. Heifers received T (35 mg i.v.) or ethanol:saline vehicle (ES) every 4 h for 44 h. All received cloprostenol (500 micrograms i.m.) immediately after the start of T or ES, and received estradiol-17 beta (500 micrograms i.m.) 12 h later. Each ES heifer had a surge of luteinizing hormone (LH) within 48 h of estradiol injection, whereas T-treated heifers did not. Estrus was observed in three ES-treated heifers, but not in T-treated heifers. In Exp. 2, 10 heifers received T (35 mg i.v.) or ES every 4 h for 64 h beginning on d 15 postestrus. Cloprostenol (500 micrograms i.m.) was injected 16 h after the start of treatment. Concentrations of LH were similar (P greater than .05) in both groups. In ES heifers, concentrations of 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM) increased; in T-treated heifers, PGFM remained at pre-cloprostenol levels. Luteolysis was induced in all heifers. Progesterone (P4) decreased to less than or equal to 1 ng/ml at similar (P greater than .05) rates in ES-treated and T-treated heifers. Mean concentration of P4 288 h post-cloprostenol was greater (P less than .05) in ES-treated than in T-treated heifers. Three ES-treated heifers, but no T-treated heifers, were in standing estrus. We conclude that T effectively antagonizes estrogen in cattle.(ABSTRACT TRUNCATED AT 250 WORDS)