Effects of progesterone and estradiol on uterine secretion of prostaglandin f(2alpha)in response to oxytocin in ovariectomized sows.

Thirty ovariectomized sows were used in an experiment designed to determine whether the ability of the porcine uterus to release prostaglandin (PG) F(2alpha) in response to oxytocin is regulated by progesterone (P(4)) and estradiol (E(2)). Sows were assigned to one of four treatment groups: 1) no steroids (ovariectomized controls; n = 8), 2) E(2) (n = 8), 3) P(4) (n = 7), or 4) E(2) + P(4) (n = 7). P(4) and E(2) were administered so as to mimic the normal temporal changes that occur in these hormones during the estrous cycle. A group of intact sows (n = 9) was included for comparison. All sows received an injection of oxytocin (30 IU, i.v.) on Days 12, 15, and 18 postestrus. Jugular venous blood samples were collected from 60 min before through 120 min after injection of oxytocin for quantification of 13,14-dihydro-15-keto-PGF(2alpha) (PGFM). Preinjection baseline concentrations of PGFM, the magnitude of the PGFM response above baseline, and area under the PGFM response curve (AUC) were calculated for each sow on each day and compared among treatment groups by ANOVA. Among the ovariectomized sows receiving steroid replacement, baseline concentrations of PGFM were low on Day 12 postestrus in all four groups. On Days 15 and 18, baseline concentrations remained low in the two groups that did not receive P(4) but increased in those that did. Both the magnitude of the response to oxytocin and AUC were small on Day 12 postestrus in all 4 groups. By Day 15, the magnitude of the response and AUC increased in the group that received both P(4) and E(2) but remained low in the other three groups. By Day 18, responses to oxytocin were greater in both groups that received P(4) than in those that did not. Baseline concentrations were similar in intact sows and in those that received both P(4) and E(2) on all three days examined. The magnitude of the response and the AUC were greater in the ovariectomized sows receiving P(4) and E(2) replacement than in the intact control sows on Days 15 and 18 postestrus. From these results, we conclude that P(4) and E(2) interact to control the time when the uterus begins to secrete PGF(2alpha) in response to oxytocin and the amount of PGF(2alpha) secreted.

Changes in uterine secretion of prostaglandin F2 alpha in response to oxytocin during the estrous cycle, early pregnancy, and estrogen-induced pseudopregnancy in swine.

Thirty-one sows were used in an experiment designed to determine whether the ability of the porcine uterus to release prostaglandin (PG) F2 alpha in response to oxytocin was suppressed in pregnancy and pseudopregnancy. Sows were assigned to one of three treatment groups: nonbred (nonpregnant) controls (n = 8), pseudopregnant (5 mg estradiol benzoate, i.m., daily on Days 11-15 postestrus; n = 8), or bred (bred once daily throughout the estrous period; n = 15). Jugular venous blood samples were collected daily for quantification of progesterone. Pregnancy was determined by uterine examination at slaughter 51-72 days postmating. On the basis of progesterone and embryo recovery, bred sows were classified into three subgroups: confirmed pregnant (n = 4), suspected pregnant based on delayed luteal regression (n = 5), or bred/not pregnant (n = 6). All sows received an injection of oxytocin (30 IU, i.v.) on Days 12, 15, and 18 postestrus. Jugular venous blood samples were collected from 60 min prior to through 120 min after injection of oxytocin for quantification of 13, 14-dihydro-15-keto-PGF2 alpha (PGFM). Magnitude of response above baseline and area under the PGFM response curve (AUC) were calculated for each sow on each day and compared among treatment groups by analysis of variance. Responses in pregnant and suspected-pregnant sows were not different on any day examined; therefore the two groups were combined (n = 9) and considered pregnant for all subsequent analyses. Responses in the nonpregnant and bred/not pregnant sows were pooled and compared to the responses in the pregnant and pseudopregnant sows. Magnitudes of response were similar between these pooled groups on Day 12 (p > 0.5), but were less in pregnant and pseudopregnant sows on Days 15 and 18 (p < 0.01). When nonpregnant and bred/not pregnant sows were compared to each other, the magnitudes of the response were similar on Days 12, 15, and 18 (p > 0.3 on each day). In contrast, when pregnant and pseudopregnant sows were compared, pseudopregnant sows had a lower magnitude of response that was consistent across all 3 days (p < 0.02). Similar relationships were apparent for the AUC. These results demonstrate that uterine secretory responsiveness to oxytocin is suppressed during early pregnancy and that this effect may be mediated through estrogen secreted by conceptuses.

Changes in peripheral concentrations of 13,14-dihydro-15-keto-prostaglandin F2 alpha induced by progesterone in swine.

This experiment was designed to examine the effects of progesterone on endogenous and oxytocin-induced secretion of prostaglandin F2 alpha (PGF2 alpha) in sows. Peripheral concentrations of 13,14-dihydro-15-keto-PGF2 alpha (PGFM) were used as an indirect measure of uterine PGF2 alpha secretion. Eight sows received twice daily injections of progesterone (160 mg/injection) on d 1 to 5 after estrus. Another eight sows received comparable injections of a corn oil injection vehicle. Each sow then received i.v. injections of oxytocin (30 IU) on d 10, 12, and 15 after estrus. Concentrations of PGFM were determined in jugular venous blood samples collected at -60, -45, -30, -15, 0, 2, 5, 10, 15, 30, 45, 60, 90, and 120 min after each oxytocin injection. The mean concentrations of PGFM in samples collected before injection of oxytocin (baseline), the magnitude of the PGFM response to oxytocin, and the area under the PGFM response curve (AUC) were calculated for the three oxytocin challenges administered to each sow. Baseline, magnitude, and AUC were low on d 10 after estrus and similar for the two treatment groups. On d 12 baseline, magnitude, and AUC remained low in the control sows; however, all three response variables increased in sows that received progesterone. By d 15, all three variables were high and similar in both treatment groups. In conclusion, progesterone, administered early in the estrous cycle, seems to promote premature secretion of PGF2 alpha as indicated by the high basal concentrations of PGFM observed before injection of oxytocin on d 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Recombinant porcine somatotropin for sows during late gestation and throughout lactation.

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.

Changes in uterine secretion of prostaglandin F2 alpha and luteal secretion of progesterone in response to oxytocin during the porcine estrous cycle.

The purpose of this experiment was to determine whether the ability of oxytocin to stimulate uterine secretion of prostaglandin F2 alpha (PGF2 alpha) and luteal secretion of progesterone changes during the porcine estrous cycle. Nineteen multiparous sows were observed for estrus. After one estrous cycle of normal length, sows were assigned randomly to receive an injection of oxytocin (30 IU, i.v.) in the EARLY (Days 4-6; n = 6), MID (Days 9-11; n = 7), or LATE (Day 15; n = 6) stage of the estrous cycle. Concentrations of 13, 14-dihydro-15-keto-PGF2 alpha (PGFM) and progesterone were determined in jugular venous serum samples collected at -60, -45, -30, -15, 0, 2, 5, 10, 15, 30, 45, 60, 90, and 120 min after injection of oxytocin. The magnitudes of the PGFM and progesterone responses and the area under the respective response curves (AUC) were calculated for each sow. Concentrations of PGFM did not change in response to oxytocin administered during the EARLY or MID portions of the estrous cycle. Concentrations increased rapidly in 4 of 6 sows that received oxytocin LATE in the estrous cycle. Both magnitude and AUC were greater LATE in the estrous cycle than at either EARLY or MID cycle (p less than 0.05). Thus, uterine secretory responsiveness to oxytocin develops between Days 11 and 15 postestrus in the sow. For progesterone, a transient increase was observed immediately following injection of oxytocin at MID cycle (p less than 0.05), but not at the other times examined. Therefore, oxytocin appears to be capable of stimulating secretion of progesterone from the functionally mature corpus luteum.

Concentrations of 13, 14-dihydro-15-keto prostaglandin F2 alpha after pulsatile progesterone administration at the time of luteolysis of heifers.

Progesterone was administered in pulses to 12 dairy heifers from days 17.5 to 22.5 post-estrus in order to determine its ability to modify secretion of PGF2 alpha around the time of luteolysis. Control heifers exhibited pulses of PGFM concomitant with a sharp decline in progesterone concentrations and thus these pulses were temporally associated with luteolysis. Additional pulses of PGFM were observed in heifers receiving exogenous progesterone, but these were not statistically predictable by either dose of progesterone (50 or 100 micrograms) or time of administration (3 or 6 hour intervals). However, all heifers (4/4) treated with progesterone at 3 hour intervals had additional pulses of PGFM as compared to only one heifer (1/4) treated at 6 hour intervals. When pulses of PGFM were induced by exogenous progesterone there was a substantial lag time between the initiation of progesterone treatment and their occurrence. The limited response to progesterone administration and the lack of synchrony is not consistent with an ability of exogenous progesterone to directly stimulate secretion of PGF2 alpha at the time of luteolysis.

Effects of estrogen and prostaglandin on progesterone-delayed farrowing.

Effects of estradiol benzoate and prostaglandin F(2alpha) (PGF(2alpha)) on concentrations of progesterone and estrogen in serum and the percentage of live births were determined in 21 gilts treated with exogenous progesterone in late gestation. All gilts received progesterone (25mg s.c. four times daily) from Days 108 through 113 of gestation. Gilts receiving no other treatments (controls) had elevated levels of progesterone through 1800 h on Day 114 (29.2 +/- 11.4 ng/ml) and farrowed at 115.6 +/- 0.3 d of gestation with a relatively low percentage of live births (66.8 +/- 17.3). Gilts treated with PGF(2alpha) administered at 0600 h on Day 114 had less (P<0.01) progesterone by 1800 h (7.0 +/- 1.3 ng/ml) relative to that of the controls, but they had similar gestation lengths (115.5 +/- 0.3) and percentages of live births (50.0 +/- 16.2). Administration of estradiol benzoate (10 mg) to gilts at 0600 h on Day 114 did not reduce progesterone on Day 114 or the gestation length relative to that of the control gilts, but it did increase (P<0.05) the percentage of live births (100%).

Effects of season and lactation on luteinizing hormone secretion in postpartum ewes.

Effects of season, postpartum interval and short-term weaning were investigated on luteinizing hormone (LH) secretion in ewes. Blood samples were collected at 10-min intervals for 4 h (basal period). Then gonadotropin-releasing hormone (GnRH) was administered and 10 more blood samples were collected over an additional 4 h period. The effects of day post partum (5, 20 or 40) and short-term weaning (weaned Day 37, tested Day 40 post partum) on basal and GnRH-induced LH secretion were tested. Mean basal concentrations of LH for ewes on Day 5, 20 or 40 post partum ranged from 1.6 to 4.6 ng/ml and did not differ. Mean concentrations of LH during the post-GnRH sampling interval were greater (P<0.01) for ewes bled on Day 20 or 40 post partum (12.3 and 11.8 ng/ml, respectively) than for ewes bled on Day 5 or for unbred control ewes (6.7 and 5.8 ng/ml, respectively). Weaning on Day 37 depressed GnRH-induced LH secretion on Day 40 post partum (8.18 ng/ml; P<0.05). Seasonal changes in LH secretion on Day 20 or 40 post partum in January, March or June lambing ewes were also tested. There was no difference in basal or GnRH-induced LH secretion between Day 20 or 40 post partum among groups in January or March.. In June, ewes had lower (P<0.01) basal and GnRH-induced LH secretion on Day 20 post partum than ewes did on Day 40 post partum. Across month of the year, on Day 20 post partum, ewes lambing in March released more LH in response to GnRH than ewes lambing in January (P=0.07) or June (P<0.05). Response to GnRH on Day 20 post partum was similar for ewes lambing in January or June (P>0.1). Ewes lambing in January released less (P<0.01) LH on Day 40 post partum than ewes lambing in March or June; however, no difference was detected between the latter two groups (P>0.1). Thus, seasonal modifications of the releasable pool of LH may mask or modify the effect of the postpartum interval upon this endocrine response.

Effects of weaning and naloxone on luteinizing hormone secretion in postpartum ewes.

The effects of weaning and naloxone on concentrations of luteinizing hormone (LH) at 20 days postpartum were examined. March-lambing Finnish Landrace x Southdown ewes (n = 20) were bled via jugular venipuncture at 10-min intervals for 4 h. Naloxone (1 mg/kg bodyweight) was administered i.v. at 60, 120, and 180 min. Treatment groups were suckled (S), weaned on Day 17 (W), suckled plus naloxone (SN), and weaned plus naloxone (WN). Mean concentrations of LH were calculated for 0-60, 70-120, 130-180, and 190-240 min time intervals. Analysis of variance indicated a group effect (p = 0.03) and a group x time interaction (p = 0.02). Concentrations of LH followed a cubic pattern in SN (p = 0.03) and WN (p = 0.08) ewes, whereas LH levels decreased (p less than 0.05) in a pattern consisting of linear and quadratic trends in S and W ewes. Concentrations of LH in S and W ewes were similar at 0-60 and 190-240 min. W ewes had lower (p less than 0.05) concentrations of LH than S ewes at 70-120 and 130-190 min. Further analysis revealed that LH was elevated in SN ewes (p = 0.01) and WN ewes (p = 0.07) at 70-120 min, but was not significantly elevated at 130-180 min. At 190-240 min LH was increased in SN ewes (p = 0.03), but LH levels in WN ewes were similar to those of SN ewes as well as to those of S control ewes.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of an estrogen antagonist (tamoxifen) on cloprostenol-induced luteolysis in heifers.

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)

Removal of swine zonae pellucidae with sequential exposures to pronase and acidified medium.

Exposure to acidified PBS (pH 3) for 60 sec removed swine zonae pellucidae from 70.4% of 27 swine morulae, and 73.7% of these formed blastocysts in culture. Further investigations revealed that treating embryos with 0.5% pronase and acidified PBS (pH 3) for 30 sec each was more effective. Zonae were removed in 90.6% of 85 embryos (four-cell to morulae) treated. A total of 76.9% of 65 zona-free embryos and 81.6% of 38 untreated embryos formed blastocysts (P>0.05). An additional 57 untreated and 49 zona-free embryos (morulae to blastocysts) were transferred to seven recipient sows. Four sows returned to estrus (18 to 27 days), but three others were pregnant when slaughtered at 38 to 42 days. One pregnant sow had received a combination of five zona-free and six untreated embryos and demonstrated the potential for further development of treated embryos in vivo.

Effect of clomiphene citrate on pituitary responsiveness to gonadotropin releasing hormone in rams and wethers.

The objective of this study was to determine the effect of clomiphene citrate (clomid) on pituitary responsiveness to gonadotropin releasing hormone (GnRH) in rams and wethers. Doses of 200 mg clomid per ram and 1 mug GnRH per 50 kg body weight were used in studies on 12 rams and 4 wethers. The experimental design involved bleeding each animal at 15-minute intervals for 6.5 hours. At the end of the first hour, GnRH was injected IV. The second GnRH challenge was administered 0.5 hours after an injection of clomid or vehicle (4.5% sorbitol solution) which was given on the third hour. The relative response to clomid or vehicle was calculated as the mean increase in concentration of LH during the two-hour period after the second GnRH injection. Each treatment (clomid and vehicle) was given to all animals with a 14-day recovery period between treatment days. The relative response for the rams receiving vehicle (1.80 +/- 0.65) was greater (P < 0.05) than the response during clomid treatment (0.34 +/- 0.22). This suppression of LH response by clomid was observed in 10 of the 12 rams. In contrast to the rams, the concentrations of LH in wethers after the second GnRH injection were lower than those observed after the first GnRH injection. Similar to the rams, the relative response following clomid treatment of wethers (0.04 +/- 0.04) was less than the relative response (P > 0.05) following vehicle (0.40 +/- 0.16). The results suggest that clomid at this dosage inhibits GnRH-induced release of LH from the pituitary of rams but not of wethers.

Dissimilarity of corpora lutea within the same ovaries or those from right and left ovaries of pigs during the oestrous cycle.

A total of 48 corpora lutea from the right and left ovaries of 2 gilts on Day 9 and 2 gilts on Day 13 of the oestrous cycle were analysed for gonadotrophin binding, progesterone concentration and 3 enzyme activities. The weights of corpora lutea from the right and left ovaries on Days 9 and 13 did not differ, but the values on Day 13 were lower than those on Day 9. The specific binding of 125I-labelled hCG, progesterone concentration, and activities of cytochrome c oxidase (a mitochondrial enzyme), beta-N-acetyl-D-glucosaminidase (a lysosomal enzyme) and glucose 6-phosphate dehydrogenase (a cytosol enzyme) differed, with some exceptions, among the corpora lutea within the same ovaries and those from the right and left ovaries on Days 9 and 13 of the cycle. The gonadotrophin binding differences amongst the corpora lutea appeared to be due to the differences in the total number of available receptors rather than in the receptor affinities. There was no strict correspondence between the magnitude of gonadotrophin binding and luteal progesterone concentration. These data show that porcine corpora lutea within the same ovaries, and those from the right and the left ovary, are quite dissimilar.

Comparison of intrauterine and subcutaneous sites of estrogen injection for luteal maintenance in swine.

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.

Change in gonadotropin-binding sites in intracellular organelles and plasma membranes during luteal growth, development and regression.

Changes in the gonadotropin-binding sites in plasma membranes and several intracellular organelles of bovine corpora lutea of days 3, 13 and 19 of the cycle were investigated. These three times represent periods of rapid luteal growth (early luteal phase), maturity (mid luteal phase) and the onset of regression (late luteal phase), respectively. The 5'-nucleotidase activity was highest in the fraction possessing a predominance of plasma membranes. It was undetectable in nuclear fractions and detectable to a varying extent in fractions enriched with mitochondria-lysosomes, rough endoplasmic reticulum and Golgi. The gonadotropin-binding sites, as measured by 125I-human choriogonadotropin (hCG) specific binding, were found in all the subcellular organelles. Whereas the affinities remained about the same, the total number of available gonadotropin-binding sites in all the organelles increased from day 3 to 13 and then declined by day 19 of the cycle. Occupancy of binding sites by endogenous luteinizing hormone was not detectable and therefore was unlikely to be responsible for the changes in total number of available binding sites. Thus, binding site changes observed in all the organelles of early, mid and late luteal phase corpora lutea probably reflect actual changes in the steady-state turnover of binding sites. Morphometrically determined relative membrane counts of various subcellular organelles varied with the luteal phase. The relative total gonadotropin-binding sites, calculated from the relative membrane counts and the total number of available binding sites, increased in all the organelles from early to mid and then declined by late luteal phase. Plasma membranes of all three luteal phases contained greater relative total gonadotropin-binding sites than any other single intracellular organelle. However, all the intracellular organelles combined contained 59% of the total luteal cell gonadotropin-binding sites in early luteal phase which decreased to 43 and 28% by mid and late luteal phases respectively.

Estrous behavior and endocrine status of dairy heifers with varied intakes of phosphorus.

We investigated whether dietary phosphorus affected estrous intensity of heifers. A total of 48 heifers (Holstein and Jersey) were allotted to diets containing approximately 73% (low), 138% (medium), or 246% (high) of the phosphorus recommended by the National Research Council. Heifers were observed continuously for 48 h beginning 36 h after an estrous-synchronizing treatment of prostaglandin F2 alpha. Heifers began standing estrus 55 +/- 12.6 h (standard deviation) after prostaglandin, with onset randomly throughout the day. Standing estrus lasted 15.4 +/- 4.1 h (standard deviation), and heifers stood to be mounted 3.68 +/- 2.38 (standard deviation) times per hour. Dietary phosphorus concentration altered inorganic phosphorus of blood serum but did not affect significantly overall estrous behavior or blood serum concentrations of progesterone, estradiol, or luteinizing hormone measured around the time of estrus. We conclude that a dietary phosphorus inadequacy as in this study does not alter reproductive endocrine function or estrous intensity in heifers.

Progesterone and estrogen concentrations in gilts with delayed parturition.

Twelve pregnant gilts were assigned to three treatments (four gilts per treatment): (1) corn oil (control) injected subcutaneously four times daily from day 110 of gestation until onset of lactation; (2) 25 mg progesterone (P4) injected subcutaneously four times daily from day 110 of gestation through day 113, or (3) 25 mg P4 injected subcutaneously from day 110 through day 115 of gestation. Excluding one gilt on treatment 2 which farrowed on day 110, average lengths of gestation for control gilts and gilts receiving treatments 2 and 3 were 113.3 +/- 1.2 (SE), 115.6 +/- .7 and 118.0 +/- .4 days. Associated mean percentages of live births were 87.4 +/- 5.9, 48.8 +/- 24.4 and 2.5 +/- 2.5, respectively. P4 averaged 2.9 +/- .6 ng/ml in blood serum of control gilts during the 24 hr preceding parturition. P4 was released in a sporadic pattern by gilts on treatment 3, resulting in higher P4 concentrations (9.0 +/- 1.7 ng/ml) for the same prepartum period. Concentrations of P4 in serum of gilts on treatment 2 averaged 7.6 +/- 1.6 ng/ml, intermediate to, but not different from, concentrations of P4 in controls and gilts on treatment 3. Concentrations of estrogen in serum of control gilts averaged 6.2 +/- 1.3 ng/ml during the 24 hr preceding parturition, whereas concentrations of estrogen in gilts treated with P4 were reduced (P less than .01) to below 2 ng/ml during the same prepartum period. The erratic pattern of concentration of P4 during and after administration of exogenous P4 may reflect a disturbance of the secretion or metabolism of endogenous P4. We suggest that failure to suppress P4 post-treatment plus reduced estrogenic stimulation impedes the birth process and contributes to the high incidence of stillbirths observed in gilts with progestin-delayed parturition.

Bovine prolactin, TSH, T and T concentrations as affected by tall fescue summer toxicosis and temperature.

Serum concentrations of prolactin (PRL), thyrotropin (TSH), thyroxine (T4) and triiodothyronine (T3) were compared between Holstein calves fed a toxic fescue (G1-307) and Holstein calves fed a less toxic fescue (G1-306) at one of three environmental temperatures (low, 10 to 13 C; medium, 21 to 23 C; high, 34 to 35 C). Three calves were assigned to each treatment combination, and hormone concentrations were determined before (basal) and after thyrotropin-releasing hormone (TRH) was injected at 15 microgram/100 kg body weight via jugular cannula. Calves fed the toxic G1-307 had lower basal PRL concentrations than those fed G1-306 (1.8 +/- .1 vs 6.0 +/- 1.2 ng/ml). Increasing ambient temperature increased basal PRL levels in calves fed G1-306 (i.e., low [2.3 +/- .3] < medium [3.6 +/- .9] < high [12.1 +/- 1.3 ng/ml]) but not in calves fed G1-307 (i.e. low [1.8 +/- .1] = medium [2.0 +/- .1] = high [1.6 +/- .1]). Similarly, after TRH injection, PRL release was greater in calves fed the less toxic G1-306 (35.7 +/- 5.2 ng/ml) than in those fed G1-307 (5.6 +/- .6 ng/ml) and was positively affected by temperature (i.e., low [6.9 +/- 1.2] < medium [18.8 +/- 5.6] < high [36.3 +/- 5.9 ng/ml]). In contrast, basal and TRH-induced TSH concentrations were unaffected by temperature or fescue. However, T3 (time 0) was inversely related to temperature (1.06 +/- .1, 1.40 +/- .1 and 1.87 +/- .2 ng/ml for high, medium and low temperature, respectively). After TRH injections, T3 increased linearly and at the same rate (.007 ng/ml/min) at all temperatures, but T4 concentrations increased only in low temperature groups. Neither T4 nor T3 concentrations were affected by forage fed. We conclude that some factor(s) in toxic fescue inhibits PRL secretion, especially at high temperature, an environmental condition closely associated with fescue summer toxicosis in cattle. Increased body temperature and respiration rates associated with fescue summer toxicosis apparently are not mediated by TSH or thyroid hormone secretion.

Effect of lactation upon the postpartum interval.

Several physiological aspects of lactation in the ewe, sow and cow were reviewed relative to possible delaying effects upon postpartum interval to ovulation, estrus and conception. Specifically considered were the possibilities that: high blood flow to the mammary gland and perturbations of that flow may disrupt vascular regulatory mechanisms in the reproductive tract, metabolism of gonadal and adrenal hormones by mammary tissue may disrupt endocrine controls essential for reproduction, suckling or milking-induced release of prolactin and oxytocin may inhibit ovarian or pituitary function and effects of social interactions associated with lactation and suckling may delay resumption of estrous cycles. The postpartum interval appears to be related to suckling intensity. An attractive hypothesis is that pituitary release of gonadotropins is inhibited during lactation as a result of pituitary desensitization to estrogen by suckling-induced surges of prolactin. Evidence for this role of prolactin is, however, circumstantial for all three species and the relationship of prolactin to the postpartum interval in cattle remains nebulous. Therefore, management practices to minimize lactational anestrus should be based upon the generalized concept that "suckling" delays postpartum cycles, rather than upon more specific hypothetical mechanisms.