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Our objective was to establish doses of orally administered NaClO3that reduced the presence of generic Escherichia coliin intestines of ewes and neonatal lambs managed in a shed-lambing system. Neonatal lambs (n = 32; age = 7.1 ± 1.2 d; BW = 6.8 ± 1.0 kg) and yearling ewes (n = 44; BW = 74.8 ± 5.6 kg) were used in 2 experiments. In both experiments, lambs and ewes were randomly assigned to 1 of 4 groups, and groups were randomly assigned to 1 of 4 treatments. In Exp. 1, neonatal lambs were given single, aqueous, oral doses of saline (control; NaCl, 30 mg·kg of BW−1) or 30, 60, or 90 mg of NaClO3·kg−1of BW. At 25.9 ± 1.3 h after treatment, lambs were euthanized, and intestinal contents were collected aseptically. In Exp. 2, ewes were given single, aqueous, oral doses of saline (NaCl, 150 mg·kg of BW−1) or 150, 300, or 450 mg of NaClO3·kg−1of BW. At 24.0 ± 0.8 h after treatment, fecal samples were collected aseptically from the rectum of each ewe. For both experiments, generic E. coliwere enumerated from intestinal contents and feces within 4 to 12 h after collection. In Exp. 1, the effect (P= 0.08) of NaClO3on the presence of generic E. coliin colon contents was dose-dependent. This effect was linear (P< 0.01) and negative, which indicated that as NaClO3dose increased, generic E. colithat could be isolated from colon contents decreased. Specifically, lambs dosed with 60 and 90 mg of NaClO3·kg−1of BW had fewer E. colicfu·g−1of content than control lambs (P< 0.06). Lambs dosed with 90 mg of NaClO3·kg−1of BW had fewer E. colicfu·g−1of content than lambs dosed with 30 mg of NaClO3·kg−1of BW (P= 0.09). Sodium chlorate dose did not influence (P= 0.58) the presence of generic E. coliin contents collected from the cecum. In Exp. 2, the effect (P< 0.0001) of NaClO3on the presence of E. coliin fecal contents from ewes was dose-dependent. This effect was quadratic (P< 0.0001) and negative; ewes dosed with 150, 300, and 450 mg of NaClO3·kg−1of BW had fewer E. colicfu·g−1of feces than control ewes. No differences in E. colicfu·g−1of feces were detected between NaClO3treatments (P= 0.88 to 0.97). Based on these results, a single oral dose of at least 60 and 150 mg of NaClO3·kg−1of BW in neonatal lambs and yearling ewes, respectively, significantly decreased the presence of generic E. coliin contents from the lower intestine.

Uterine infections (i.e., endometritis) can have a major economic impact on dairy production. Identifying cows that are susceptible to endometritis and improving the diagnosis of endometritis could lead to a reduction in the impact of such infections. Thus, we used Holstein cows to determine whether postpartum changes in 13, 14-dihydro-15-keto-PGF2alpha (PGFM), a metabolite of PGF2alpha, could be used to identify cows that are susceptible to endometritis and to improve the diagnosis of endometritis. Cows were assigned to three treatments. 1) Control (n = 10) had no clinical or bacteriological signs of endometritis during the study. 2) Treated (n = 11) developed endometritis spontaneously and were treated i.m. with 25 mg of PGF2alpha immediately after clinical diagnosis (d 17.6 +/- 0.8 postpartum; mean +/- SEM). 3) Untreated (n = 10) developed endometritis spontaneously and were not treated after diagnosis (d 20.0 +/- 0.5). Examinations of external and internal genitalia and bacteriological data were used to diagnose endometritis. From d 0 (calving) until approximately d 63 postpartum, jugular blood was collected three times weekly. Progesterone and PGFM were quantified in plasma. For PGFM, the treatment x day interaction was significant (P< 0.01). Overall PGFM profiles for Control and Treated differed (P< 0.05), but the Untreated profile did not differ from either Control or Treated. To better understand the interaction, PGFM data from d 0 to 35 postpartum were partitioned into consecutive 7-d periods, and d-36 and greater data were partitioned into one period. Effects of treatment, day, and the treatment x day interaction were then evaluated within period. Except for the d-15 to -21 period, PGFM was greater (P< 0.03) in Control than in Treated and Untreated. In Treated and Untreated, PGFM increased during the d-15 to -21 period. For progesterone, treatment did not affect the profiles, but day was significant (P< 0.001). Progesterone concentrations were basal from d 0 until approximately d 12, and they generally increased after d 12. Onset of endometritis was associated with increased progesterone concentrations. Treatment did not affect the interval from calving to first detected estrus (29.5 +/- 4.9 d) or from calving to AI (73.3 +/- 8.7 d). We conclude that PGFM measures have the potential to be used to identify cows that are more likely to develop endometritis and that PGFM may aid in the diagnosis of endometritis.

Two experiments were designed to examine whether hormonal profiles were related to luteal life span in pluriparous postpartum anestrous beef cows. Cows (Exp. 1, n = 34; Exp. 2, n = 23) received norgestomet (N) for 9 d or served as controls (C). Each cow received 1,000 IU human chorionic gonadotropin (hCG) 48 h after removal of N (d 0). Blood samples collected every 15 min for 8 h on d −5, 3 and 5 (Exp. 1) or on d −10 and −1 (Exp. 2) were assayed for luteinizing hormone (LH) and follicle stimulating hormone (FSH). Cortisol was determined in hourly samples collected on d −5 and in samples collected every 2 min during suckling on the same day (Exp. 1). Concentrations of 15-keto-13,14-dihydro-PGF2α (PGFM) were determined in samples collected at 15-min intervals for 2 h on d −5, 3, 5 and 10 (Exp. 1). EstradioI-I7β was measured in samples collected on d −5 (Exp. 1) or on d −10 and −1 (Exp. 2). Life span of induced corpora lutea was longer (P<.05) in N than C cows. Percentages of N cows in which corpora lutea, formed in response to hCG, exhibited a normal life span were 83% on farm 1 and 25% on farm 2 (Exp. 1), and 90% (Exp. 2), compared with 0% in C cows. Concentrations of FSH were not affected by N but were lower (P<.05) on d −5 in cows on farm 2 (.6 ± .1 ng/ml) than in cows on farm 1 (.8 ± .1 ng/ml). On d −5, a treatment × farm interaction (P<.05) for mean LH was observed and frequency of pulses of LH was higher (P<.01) in N than C cows (2.7 ±.4 vs .8 ± .8 pulses/8 h). Neither Cortisol nor PGFM was affected by N. Estradiol was increased in d −1 (6.1 ± .5 vs 2.6 ±.8 pg/ml; P<.01) by N. It is suggested that pre-treatment with N enhanced life span of induced corpora lutea, in part, by influencing secretion of LH and development of follicles, but a threshold concentration of FSH was required for N to exert this effect.

The effect of an intrauterine device (IUD) on uterine release of PGF2α was studied in gilts. An IUD (15 × 75 mm plastic coil) was inserted at the mid-point of one uterine horn on day 3 of an estrous cycle in seven gilts and inserted and removed immediately in six sham-operated gilts. At relaparotomy on day 6, uterine venous blood samples were collected from uterine branches of the ovarian veins draining three separate sites of the uterine horns. One sample was from the area of the uterine horn that received the IUD or sham operation, one anterior to the IUD site on the same uterine horn and one at the midpoint of the opposite uterine horn. These plasma samples were radioimmunoassayed for PGF2α. Estrous cycle lengths of gilts which received an IUD (20.1 ± .5 days) were not different from those of the sham-operated gilts (24.1 ± 2.6 days; P>.1). Values for PGF2α exhibited heterogeneity of variance among groups. At the IUD site, mean concentration of PGF2α (ng/ml) was 14.0 ± 7.3 in IUD-treated gilts and 3.6 ± 1.7 in sham-operated gilts. When one high value at the IUD site (57 ng/ml) was excluded from analysis, variances were not heterogeneous and concentration of PGF2α at the IUD site (7.1 ± 1.9) was higher than in the control gilts (3.6 ± 1.7; treatment × site interaction, P>.01). The concentration of PGF2α in uterine venous plasma collected from the midpoint of the opposite uterine horn (4.2 ± .9 vs2.5 ± 1.0) or anterior to the IUD on the same horn (2.0 ± .9 vs3.4 ± 1.6) were not different between IUD-treated and sham-operated gilts, respectively. An IUD has a very localized stimulatory effect on uterine synthesis of PGF2α in gilts

Regulation of the secretion of estradiol-17β after exogenous prostaglandin F2α (PGF2α) and the luteolytic potential of intrafollicular PGF2α were examined in beef heifers. Hereford heifers were observed for estrus twice daily, and after two normal estrous cycles were assigned to randomized treatments on day 11 postestrus.In Experiment I, the largest follicle on the ovary with the corpus luteum (CL) received a 50 µl injection of PGF2α (600, 900, 1,200 µg), Tham buffer (TB) or TB plus removal of the CL (six heifers per group). Lengths of estrous cycles (days) of heifers treated with 600 µg PGF2α (19.0 ± 1.5) or TB (20.0 ± .5) did not differ. Lengths of cycles for heifers receiving 900 (14.5 #x00B1; .5) and 1,200 µg PGFF2α (15.0 ± .2) or TB plus removal of the CL (14.0 ± .5) were not different, but were shorter (P<.01) than estrous cycles in the other groups. Declines in the concentrations of systemic progesterone among heifers receiving 900 or 1,200 µg PGFF2α did not differ from those in heifers receiving TB plus removal of the CL, but were not parallel to the profiles of systemic concentrations of progesterone in heifers receiving TB only (P<.01). Profiles of progesterone in heifers receiving 600 µg PGF2α differed from those in heifers receiving either TB only or TB plus removal of the CL. Increasing concentrations of estradiol-17β were observed only when concentrations of progesterone declined to low levels. Profiles of estradiol-17β were parallel among heifers receiving luteolytic doses of PGFF2α (900 or 1,200 µg) or TB plus removal of the CL, but differed from those in heifers receiving TB only. Changes in concentrations of luteinizing hormone (LH) were observed after concentrations of progesterone declined and before increases in concentrations of estradiol-17β. Profiles of the concentrations of estrone did not vary among treatments.In Experiment 2, the corpus luteum was removed from 12 heifers on day 11 postestrus. Six of the heifers were anesthetized with sodium pentobarbital from 4 to 10 hr after removal of the CL. Pentobarbital blocked the changes in concentrations of LH, compared to unanesthetized control heifers. However, the profiles of estradiol-17β in heifers receiving pentobarbital were parallel to those observed in unanesthetized heifers. It is suggested that increases in the concentrations of estradiol-17β occur in response to withdrawal of progesterone without any detectable direct influence of exogenous PGF2α. Until 24 hr after removal of the CL these increases in estradiol occurred independently of changes in the concentrations of LH.

In three experiments, we examined the effects of suckling, progestogen treatment, hysterectomy or exogenous gonadotropin releasing hormone (GnRH) on ovarian function in autumn-lambing, postpartum ewes. In each experiment, GnRH was injected on approximately d 25 postpartum. Suckling reduced (P<.01) GnRH-induced release of luteinizing hormone (LH) but not of follicle stimulating hormone (FSH), and reduced (P<.05) the proportion of ewes that developed corpora lutea in response to GnRH. Suckling had no effect on duration (8.8 d) of GnRH-induced luteal phases. Progestogen prior to GnRH increased (P<.01) the duration of the first luteal phase (10.1 vs 7.6 d; progestogen-treated ewes vs control ewes), but progestogen did not affect the release of LH or FSH. Progestogen treatment did not alter the interval from parturition to the first detected estrus (42.6 d). The concentration of 13,14-dihydro-15-keto-PGF2α (PGFM) just after lambing was >400 pg/ml of jugular plasma, but concentrations of PGFM declined thereafter. Hysterectomy the day after lambing hastened (P<.001) the decline in concentrations of PGFM, indicating that prostaglandins from the postpartum uterus probably caused the high concentrations of PGFM in jugular plasma. Hysterectomy reduced (P<.05) the interval from parturition to detectable luteal function (19.6 vs 25.3 d) and enhanced (P<.001) luteal production of progesterone. This study of autumn-lambing ewes indicates that the uterus has a negative effect on ovarian function and that suckling and progestogen affect ovarian response to GnRH.

Effects of heat stress during the last third of gestation on reproductive changes postpartum were studied in Holstein cows. Cows and heifers 160 to 190 d of gestation were assigned in June 1978 to shade (n = seven cows and two heifers) or no shade (n = eight cows and two heifers) management treatments. After parturition, all cows (n = 19) were moved to the milking herd and managed uniformly. On the day of calving and on each Monday, Wednesday and Friday thereafter until d 50 postpartum, jugular blood samples were collected. Beginning approximately 7 d postpartum, the reproductive tract of each cow was examined rectally after collection of blood samples. Estrus was monitored twice daily and cows were inseminated after d 45 postpartum. Prepartum heat stress increased 13,14-dihydro-15-keto-prostaglandin F2α (PGFM) concentrations postpartum and increased the rate of uterine involution. Regardless of prepartum treatment, progesterone concentrations indicated that luteal phases had begun by d 12.4 ± 1.3 postpartum, which was about 3 d before PGFM was basal. The first luteal phase lasted only 10.7 ± .9 d. First estrus was not detected until d 32.3 ± 4.8 postpartum. The previously gravid uterine horn had a negative effect on ovarian volume, diameter of the largest follicle and percentage of ovaries with a corpus luteum. However, prepartum heat stress attenuated this effect. This study indicates that heat stress prepartum had residual effects on postpartum reproductive changes, and that the previously gravid uterine horn exerted some control, which was attenuated by heat stress, over ovarian recrudescense. Even though heat stress prepartum affected sensitive measures of postpartum reproductive function, it did not alter days to first estrus, days open (102.3 ± 13.1) or services/conception (2.5 ± .3).

Postpartum changes in concentrations of 13, 14-dihydro-15-keto-prostaglandin F2α (PGFM) and progesterone and gonadotropin-releasing hormone (GnRH) induced release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in two experiments on suckled and nonsuckled autumn-lambing ewes. In both experiments, one group of ewes had lambs weaned on d 3 ± .5 postpartum and was compared with a second group of ewes that suckled one lamb each. In Exp. 1, jugular blood samples were collected daily from the day after lambing until d 50 postpartum for assay of PGFM and progesterone. On d 21 ± .5 postpartum, ewes (eight suckled and eight nonsuckled) received GnRH (100 µg), and LH and FSH were measured in blood samples collected over a 340 min period. In Exp. 2, jugular blood samples were collected from the day of lambing until d 22 ± .6 postpartum for assay of PGFM and progesterone. Ewes (six suckled and seven nonsuckled) received GnRH (100 µg) on d 22 ± .6 postpartum, and LH and FSH were quantified in blood samples taken over a 185 min period. The pituitary was removed from each ewe 190 min after GnRH for LH and FSH determinations. Postpartum changes in concentrations of PGFM and progesterone did not differ with suckling in either experiment. In both experiments PGFM concentrations were high on d 1 postpartum, but declined to basal values by d 11. The release of LH after GnRH in Exp. 1 was greater (P<.001) in suckled than in nonsuckled ewes. In Exp. 2, LH release after GnRH was not affected by suckling, but in both experiments suckled ewes had a greater (P<.01) release of FSH than did nonsuckled ewes. Pituitaries from suckled ewes contained more FSH (P<.01) than pituitaries from nonsuckled ewes. The resumption of ovarian cyclicity in well-fed autumn-lambing ewes appeared to be neither altered by suckling nor limited by the ability of the pituitary to respond to GnRH.

Effects of Syncro-Mate B (SMB) and(or) short-term calf removal (CR) on pituitary and ovarian responses after gonadotropin releasing hormone (GnRH) were studied in two experiments. In Exp. 1, 24 thin, 2-yr-old, anestrous, Brahman crossbred cows were allotted randomly to a 2 × 2 factorial design involving 27-h CR and SMB. All cows were injected (iv) with 150 µg GnRH at 24 h after removal of implants and(or) calves. Blood samples were collected at −30, 0, 15, 30, 45, 60, 90, 120 and 180 min post-GnRH. The GnRH-induced release of luteinizing hormone (LH) differed among treatments (P<.05). The release of LH was higher in cows with CR than in control cows (P<.05). Although pretreatment with SMB increased the quantity of LH release compared with the CR and control cows, SMB + CR did not show an additive effect over SMB alone. In Exp. 2, 49 mature Charolais × Hereford cows were allotted randomly to one of the following groups: control, 24-h CR or 32-h CR. Follicular size was measured by palpation per rectum at the time of CR. All cows received 300 jug GnRH (im) at 24 h after CR, at which time calves were returned to cows in the 24-h CR group. The pattern of release of LH over time was similar to the control and 24-h CR groups; however, LH release was greater (P<.05) in the 32-h CR group. A linear effect of follicular size on the pattern of release of LH after GnRH injection was observed regardless of treatment. Plasma concentration of progesterone at 7 and 14 d after GnRH, indicated that function and lifespan of the induced corpora lutea were not altered by CR or follicular size. These results indicate that pretreatment with SMB increased the release of LH to exogenous GnRH. Furthermore, CR also increased the responsiveness of the pituitary to GnRH, provided that the calves were not returned during the period of induced LH release.

Two experiments were conducted with multiparous, anestrous ewes of mixed breeding that lambed in the autumn. Ewes in each experiment were assigned randomly to treatments in a 2 × 2 factorial arrangement. Ewes in groups 1 and 2 received flurogestone acetate from an intravaginal pessary (containing 20 mg) during days 17 to 21 postpartum, while ewes in groups 3 and 4 received no progestogen. Lambs of ewes in groups 2 and 4 were weaned on day 20 postpartum. All ewes received 150 μg of gonadotropin releasing hormone (GnRH) in a single IM injection on the morning of day 22 postpartum. In Exp. 1, jugular blood was collected just before GnRH and at 30-min intervals over the next 3 hr to monitor release of luteinizing hormone (LH). Jugular blood was collected from each ewe in Exp. 2 just before GnRH and daily for the next 16 days for determination of progesterone. Seven days after treatment with GnRH, all ewes were laparotomized, ovaries were observed and uterine blood samples were collected for assay of prostaglandin F2α (PGF2α). Ewes in Exp. 2 were checked for estrus at 12-hr intervals beginning the morning after GnRH and were bred when found in standing estrus. Mean concentrations of LH (nanograms/milliliter) during the 3-hr test period were higher (P<.05) in progestogen-treated (59.2) than in control (39.5) ewes. Pattern of release of LH after GnRH was altered by progestogen treatment (P<.01; progestogen × time interaction) but not by the number of lambs suckling before or after day 20 postpartum. Profiles of progesterone over time after GnRH varied with progestogen treatment (P<.01), but not with number of lambs suckling before day 20 or weaning on day 20. Mean concentrations of progesterone (nanograms/milliliter) varied (P<.05) with the number of lambs suckling before day 20 (2.3, 1.6 and .6 for ewes suckling one, two and three lambs, respectively). All ewes had corpora lutea (mean = 2.6) at laparotomy. The life of induced corpora lutea in Exp. 2 averaged 11.8 days and did not vary significantly with treatment. Ewes showed estrus and were mated an average of 17.7 days after GnRH, and 82% lambed to this mating. Concentrations of PGF2α were lower (P<.05) in ewes receiving progestogen than in those not receiving progestogen (1.7 vs4.2 ng/ml), but were not affected by number of lambs suckling before or after day 20 postpartum. Weaning of lambs and treatment for 4 days with progestogen did not improve life span or function of corpora lutea induced by GnRH. Variation in duration of luteal function after GnRH could not be explained by the pattern of release of LH after GnRH or by concentrations of PGF2α in uterine venous plasma 7 days after GnRH.

The effects of early pregnancy on tissue concentrations of prostaglandins E2and F2α: (PGE2and PGF2α) in the ovine endometrium, uterine vein and ovarian artery and on concentrations of PGE2and PGF2α in uterine venous plasma were examined. The relationship of concentrations of progesterone in jugular plasma to concentrations of PGE2and PGF2α in uterine venous plasma was determined. A uterine branch of the ovarian vein (UBOV) adjacent to an ovary bearing a corpus luteum was cannulated on day-14 postestrus in four pregnant and five nonpregnant ewes. Blood was collected from the UBOV of each ewe at 30-min intervals during each of five collection periods lasting approximately 1 hr (three blood samples per period; 15 per ewe). The first collection of blood from the UBOV was initiated at 0700 hr on day-15 postestrus. Each successive collection period was initiated approximately 6 hr after the start of the previous period. A jugular blood sample was taken from each ewe immediately after each sample from the UBOV. Samples of endometrium, uterine vein and ovarian artery were collected from each ewe on the morning of day-16 postestrus.The overall mean concentrations (ng/ml) of PGE2(.7 ± .1 vs1.2 ± .2) and PGF2α (3.3 ± .4 vs4.4 ± .9) in plasma from the UBOV and progesterone (3.1 ± .1 vs2.4 ± .1) in jugular venous plasma did not differ in pregnant and nonpregnant ewes. Profiles of PGE2did not differ with pregnancy status. Profiles of PGF2α differed over the 24-hr period studied (pregnancy status × collection period; P<.05), but not within the collection periods. Concentration of progesterone decreased significantly over time (P<.05) and collection periods (P<.01) in the nonpregnant ewes, but showed no covariance with concentrations of PGF2α and PGE2in pregnant or nonpregnant ewes.Concentrations of PGE2and PGF2α in endometrium and uterine venous tissue and PGF2α in ovarian arterial tissue were not affected by pregnancy status. In ovarian artery there tended to be less PGE2in nonpregnant than in pregnant ewes (P<.01).

Three experiments were conducted to examine the effects of early pregnancy on levels of prostaglandin F2α (PGF2α) in the ovineendometrium and on concentrations of PGF2α, 15-keto-PGF2α and 13, 14-dihydro-15-keto-PGF2α in uterine and jugular venous plasma. In the first study, content (ng) and concentration (ng/g) of PGF2α were found to be greater in the endometrium of pregnant (1,996 ± 256 and 179 ± 29, respectively) than of nonpregnant (1,046 ± 145 and 91 ± 14, respectively) ewes, particularly on days 15 and 16, but no change was detected in concentrations of PGF2α in uterine venous plasma (5.8 ± 1.3 and 5.6 ± .8 ng/ml, respectively). Of the two metabolites of PGF2α measured in jugular plasma, only 15-keto-PGF2α was detectable, which may indicate that the ewe lung lacks the Δ 1 3-reductase enzyme. Both 15-keto-PGF2α and 13, 14-dihydro-15-keto-PGF2α were detectable in uterine venous plasma, but no differences in the concentrations of these metabolites were found between pregnant and nonpregnant ewes. In the second study, patterns of concentrations of PGF2α in plasma were parallel between left and right uterine branches of ovarian veins (UBOV) in nonpregnant ewes on days 7 and 13 postestrus. Profiles of PGF2α were essentially parallel in plasma from the left and right UBOV among pregnant and nonpregnant ewes on day 15 postestrus in the third experiment. Number and frequency of peaks of PGF2α were not different in plasma from left and right UBOV among nonpregnant ewes on days 7 and 13 or among pregnant and nonpregnant ewes on day 15 postestrus. It is concluded that prevention of luteolysis in the pregnant ewe cannot be explained entirely by changes in patterns of concentrations of PGF2α or its primary metabolites in uterine venous plasma.

Transfer of prostaglandin F2α (PGS2α) from an injected follicle to a corpus luteum (CL) in the same ovary was examined. All ewes were unilaterally-ovariectomized and the remaining ovary was either bisected and reconstructed with a latex septum or marked with India ink in the plane of bisection (sham-operated) on day-3 postestrus. An intrafollicular injection (20 µ1) was made on day 9 according to the following randomized treatments: Bisected ovary plus PGF2α (250 ;µg) in the half of the ovary containing the CL (adjacent; four ewes) or opposite to the CL (three ewes); bisected ovary plus Tham buffer (four ewes); sham-operated plus PGF2α (six ewes) or Tham buffer (six ewes). Length of estrous cycles (days) for ewes in which the ovary was bisected plus PGF2α adjacent to the CL (12.1 ± 4), bisected plus PGF2α opposite to the CL (11.5 ± .8) and sham-operated plus PGF2α (11.9 ± 3) did not differ. However, they were shorter (P<.01) than cycles of ewes with bisected ovaries plus buffer (17.5 ± .5) or sham-operated plus buffer (16.8 ± .3). Prior to injection on day-9 postestrus, ewes with bisected ovaries had lower (P<.05) jugular venous progesterone (1.3 ± .3 ng/ml) and higher luteinizing hormone (LH; 3.3 ± 1.7 ng/ml) than ewes with sham-operated ovaries (2.7 ± .3 and .4 ± .1, respectively). Concentrations of estradiol-17ß (pg/ml) on day 9 were not different in ewes with bisected (3.4 ± .8) or sham-operated (2.7 ± .3) ovaries.The profiles of progesterone decline over time were similar in all ewes injected with PGF2α regardless of surgical treatment or site of injection but were not parallel to those observed in buffer-treated ewes. Concentrations of estradiol-17ß increased only when concentrations of progesterone declined to low levels following injection of PGF2α. It is suggested that PGF2α injected into a follicle in an ovary bearing a corpus luteum is luteolytic through a local extra-ovarian pathway.Follicles (≥2mm) were recorded at each laparotomy by location relative to the corpus luteum as a preliminary examination of a possible local relationship between corpora lutea and follicular development in ewes. Bisected ovaries had fewer (P<.01) total follicles and fewer follicles 2 to 5 mm than sham-operated ovaries on days 3 and 9. On day 9 there were more follicles ≥5 mm and greater follicular volume in the half of the ovary containing the corpus luteum (P<.05) in bisected or sham-operated ovaries. However, a greater mean follicular diameter adjacent to the CL (P<.05) was evident only in bisected ovaries on day 9. It is suggested that corpora lutea may influence follicular growth locally within the ovary.

Multiparous Angus and crossbred Angus cows were used to determine the effect of induced endometritis on plasma concentrations of 13,14-dihydro-15-keto-prostaglandin F2α(PGFM) and progesterone (P4) and on duration of the estrous cycle of treatment. Beginning on the day of calving (d 0), blood samples were collected on alternate days. On three consecutive days, ranging from d 8 to 14 of the first postpartum estrous cycle, uterine horns were inoculated transcervically with either 3 × 109colony forming units (cfu) of Actinomyces pyogenesand 1.5 × 109cfu of β-hemolytic Escherichia coli(treated; n = 9) in sterile PBS or with sterile PBS alone (control; n = 9). Samples of uterine fluid were collected by transcervical aspiration twice weekly from just before the start of each series of inoculations until the end of the experiment. Endometrial biopsies were collected transcervically between d 4 to 6 and 11 to 13 after inoculation. Based on clinical observations and results of bacterial cultures, all treated cows developed acute uterine infections. Controls did not develop uterine infections. Endometrial biopsies indicated that there were no significant diffuse or focal cellular reactions in response to the infection. The interestrous interval was greater (P< .0003) for treated (27.7 ± 1.0 d) than for control (20.6 ± 1.0 d) cows, but P4concentrations were similar between the two groups. Mean PGFM concentration and PGFM profiles were similar (P> .10) between treated and control cows before bacterial infusions. Bacterial infusions increased mean PGFM concentration (P< .0001) and changed the shape of the PGFM profile (P< .02).(ABSTRACT TRUNCATED AT 250 WORDS)