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D R Deaver

Publications and source records attributed to D R Deaver.

46 records · Page 3Linked to original sources

Endocrine profiles associated with life span of induced corpora lutea in postpartum beef cows.

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-PGF2 alpha (PGFM) were determined in samples collected at 15-min intervals for 2 h on d -5, 3, 5 and 10 (Exp. 1). Estradiol-17 beta 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 less than .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 less than .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 X farm interaction (P less than .05) for mean LH was observed and frequency of pulses of LH was higher (P less than .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 less than .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.

Anestrus↗

Relationships between LH and estradiol-17 beta after removal of luteal progesterone in the ewe.

Three experiments were conducted to examine the relationship between systemic concentrations of luteinizing hormone (LH) and estradiol-17 beta (E2) after withdrawal of progesterone in cycling ewes. In Exp. 1, ewes were assigned randomly to one of three treatments: laparotomy (C), removal of the luteal ovary (ULO), or ULO plus anesthesia with sodium pentobarbital for 6 h beginning 4 h after surgery. Anesthesia was used in an attempt to block the expected increase in tonic secretion of LH. Patterns of LH and E2 in these three groups did not differ during the 24-h experimental period. In Exp. 2, a longer period of anesthesia was utilized. Forty-eight ewes were assigned at random to one of four treatments: C, ULO, lutectomy or an intrafollicular injection of prostaglandin F2 alpha (PGF2 alpha). One-half of the ewes in each group were anesthetized with sodium pentobarbital from initiation of treatment (0 h) until 10 h after surgery. Sodium pentobarbital did not suppress the increases in LH and E2 after progesterone withdrawal. The regression of concentrations of E2 on concentration of LH was not significant. In Exp. 3, ewes were infused with either saline or dopamine after receiving an im injection of PGF2 alpha. Tonic secretion of LH increased after 4 h in ewes infused with saline, but not in ewes infused with dopamine. Despite the suppression of LH, concentrations of E2 increased in dopamine-treated ewes as in control ewes. Therefore, the initial increase in E2 after a decline of progesterone in cycling ewes is independent of increases in LH.

Anesthesia↗

Effects of dopamine and serotonin on concentrations of luteinizing hormone and estradiol-17 beta in plasma of cycling ewes.

Effects of 0, 0.66 and 6.6 micrograms/kg per min of dopamine (DA) and of 0, 0.06 and 0.66 micrograms/kg per min of serotonin (5-HT) on secretion of luteinizing hormone (LH), estradiol-17 beta and progesterone were examined in ewes during luteal regression and the follicular phase. Onset of luteolysis was synchronized with two injections of 7.5 mg prostaglandin F2 alpha (PGF2 alpha) (i.m.) given 3 h apart in ewes which were 12-14 days postestrus. Ewes were infused intravenously with DA, 5-HT or a combination of DA and 5-HT for a 60-h period beginning at the time of the first PGF2 alpha injection. Neither DA nor 5-HT influenced the decrease in plasma concentrations of progesterone following PGF2 alpha. Effects of DA and 5-HT on tonic secretion of LH changed during the infusion. During the first 12 h, increasing doses of DA depressed and increasing doses of 5-HT increased mean concentrations of LH in plasma in a linear manner (DA, P less than 0.01; 5-HT, P less than 0.05). Between 16 and 34 h, 6.6 micrograms/kg per min of DA continued to suppress LH, however, 5-HT was no longer stimulatory to secretion of LH. DA was unable to inhibit secretion of LH after 40 h. Also, between 0 and 34 h, concentrations of estradiol-17 beta in plasma were decreased by infusion of DA (P less than 0.01). Interval from PGF2 alpha to onset of the preovulatory surge of LH, magnitude of the surge and duration of the surge were not altered by infusion of either DA or 5-HT.

Animals↗

Effects of ovarian secretions and dopamine on secretion of luteinizing hormone and prolactin in ewes.

In the present study, effects of dopamine (DA) and ovarian secretions on release of luteinizing hormone (LH) and prolactin (PRL) were examined using two methods of withdrawal of progesterone. Eight to 10 d after estrus, 36 ewes were assigned to one of six treatments: 1) lutectomy; 2) lutectomy and DA; 3) ovariectomy; 4) ovariectomy and DA; 5) ovariectomy and estradiol-17 beta or 6) ovariectomy, estradiol-17 beta and DA. Estradiol-17 beta was administered by Silastic implants inserted during surgery. Immediately after surgery, ewes were infused iv with DA (6.6 micrograms X kg-1 X min-1) or saline for 48 h. Infusion of DA did not affect secretion of LH after surgical removal of the corpus luteum. In lutectomized ewes, concentrations of LH in serum increased between 0 and 12 h from .5 to 3.3 ng/ml, declined between 12 and 16 h and then plateaued at 1.1 to 1.5 ng/ml. In contrast, concentrations of LH in ovariectomized ewes increased between 0 and 12 h and then remained at 3 to 5 ng/ml. Surges of LH occurred between 40 and 50 h postsurgery in eight of 12 lutectomized ewes, 11 of 12 ovariectomized ewes with implants of estradiol-17 beta and zero of 12 ovariectomized ewes. The magnitude of the surge of LH was higher in lutectomized ewes than in ovariectomized ewes with implants of estradiol-17 beta. Infusion of DA inhibited release of PRL, but there was no effect of method of progesterone withdrawal. Lutectomized ewes, but not ovariectomized ewes with implants of estradiol-17 beta, had a surge of PRL associated with the surge of LH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Estrone concentration in the peripheral plasma of pregnant and non-pregnant gilts.

A rapid radioimmunoassay for estrone (total unconjugated and sulfated) was developed to determine plasma estrone (E1) concentrations in inseminated gilts that conceived and those that had not. Thirty-one 160 day-old prepuberal gilts were induced to ovulate with gonadotropins and were artificially inseminated 10 hr before the expected time of ovulation (Day 1 - day of insemination). Unconjugated E1 and E1SO4 were extracted from 20 to 500 microl of plasma twice with 5 ml of tetrahydrafuran:ethyl acetate (1:1). Aliquots of a standard E1SO4 preparation were dissolved in 500 microl of distilled water and extracted at the same time as the plasma samples. The dried extracts were solvolyzed for 1 hr at 50 degrees C in 0.6 ml of glacial acetic acid:ethyl acetate (1:1), and the dried residue was redissolved in 0.2 ml of distilled water and extracted once with 2 ml of diethyl ether. Twenty of 31 gilts were pregnant at Days 29 to 31 of the induced cycle. Plasma E1 in pregnant gilts increased from 85 pg/ml on Day 18 to 702, 1879 and 2793 pg/ml, respectively, on Days 22, 25 and 29 to 31. Three of the non-pregnant gilts had plasma progesterone secretion maintained until Day 22; they also had a transitory increase in plasma E1 on Day 22 (215 pg/ml). Some blastocysts may have been present to exert a temporary luteotropic effect, but not enough blastocysts to completely overcome the luteolytic effect of the uterus. Quantification of plasma E1SO4 could be used as a pregnancy test in the pig.

Journal Article↗

Differential control of placental lactogen release and progesterone production by ovine placental tissue in vitro.

The hypothesis that placental secretion of progesterone (P4) and ovine placental lactogen (oPL) are controlled through different mechanisms was tested. Placental tissue was obtained at days 133-138 of pregnancy, and explant incubations were established using 200 mg tissue per flask in 5 ml O2-saturated DMEM containing 24 mM HEPES and lacking phenol red (pH 7.4). Following a 30-min preincubation, and a 15-min control period, test substances were added and incubations continued, with periodic gassing, for 4 h at 37 degrees C in a shaking water bath. Dopamine (DA), norepinephrine (NE) and epinephrine significantly stimulated P4 production (P less than 0.05). The enhancement of placental P4 production was mimicked by the addition of 8-bromo-cyclic adenosine monophosphate and forskolin (P less than 0.05). The response to catecholamines was abolished by the addition of propranolol (P less than 0.05) but not by phentolamine (P greater than 0.05). Inclusion of a membrane-permeant substrate for P4 synthesis, 25-hydroxycholesterol, increased basal (P less than 0.05) but did not enhance agonist-induced P4 production (P greater than 0.05). High performance liquid chromatographic analysis of placental tissue demonstrated the presence of DA (80.8 +/- 7.07 pg/mg) and NE (48.8 +/- 5.77 pg/mg), as well as catecholamine metabolites. Addition of 1,2-dioctanoyl-sn-glycerol (DAG) or phorbol 12-myristate-13-acetate (PMA) enhanced oPL secretion (P less than 0.05) without affecting P4 production. The response to DAG and PMA, representing the release of considerably more oPL than can be detected by extracting the tissue, was not influenced by treatment with cycloheximide (P greater than 0.05) indicating that secretion of preformed oPL is regulated by the protein kinase C pathway. These results support the hypothesis that the secretion of oPL and the production of P4 are controlled by different mechanisms.

8-Bromo Cyclic Adenosine Monophosphate↗

Effects of recombinant bovine somatotropin on luteinizing hormone and ovarian function in lactating dairy cows.

Thirty-two lactating Holstein cows were assigned to 1 of 4 groups in a randomized block design using a 2 X 2 factorial arrangement of treatments. Recombinant bovine growth hormone (rbSt; 25 mg/day) or placebo was administered beginning at Day 35 or 70 postpartum. All cows began treatment approximately 3 days post-estrus. Blood samples were collected at least once daily for a 70-day period to determine the concentration of progesterone and the duration of the luteal and follicular phases. During estrous cycles 1 and 3, frequent blood samples were taken (every 10 min for 8 h) 24 and 60 h after the onset of luteal regression. These samples were assayed for luteinizing hormone (LH), and samples coincident with the second LH pulse detected were assayed for estradiol. Ultrasonography was used to determine the size of the largest ovarian follicle from Day 17 until ovulation in estrous cycles 1 and 3. Luteal life span, length of the follicular phase, and diameter of the largest follicle were not affected by treatment with rbSt. Administration of rbSt increased the concentration of progesterone in plasma during the first two luteal phases (p less than 0.01). Progesterone was elevated during the mid-luteal phase of cycle 3 in rbSt-treated cows that began treatment about Day 35 postpartum but not in cows that began treatment on Day 70 postpartum (Treatment X Stage X Day, p less than 0.01). During the first follicular phase studied, LH pulse frequency was higher (p = 0.06) in rbSt-treated cows than in cows receiving the placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of caudal elevation on testicular function in rats. Separation of effects on spermatogenesis and steroidogenesis.

A variety of biologic processes are perturbed when exposed to microgravity (space flight) for more than 7 days, including testicular function. Suspension of rats in a special harness (caudal elevation) to induce thoracic pooling of blood fluids and remove the support function of the hind limbs is used to mimic, on earth, the effects of microgravity encountered during space flight. Typically, this induces cryptorchidism in male rats. Three experiments were conducted to differentiate the effects of caudal elevation (30 degrees angle) and anatomic location of testes on spermatogenesis and steroidogenesis. Rats were subjected to caudal elevation for 7 days using either a tail harness (experiments 1 and 2) or a whole-body harness (experiment 3). Testes of rats fell into the abdominal cavity when a tail harness was used, but ligation of the inguinal canal prevented this repositioning. For rats with abdominal testes, testicular weight was reduced (P less than 0.05) and histology of testes was abnormal; the number of spermatids per gram parenchyma was lower (P less than 0.05) in tail-suspended rats compared with control rats. In contrast, spermatogenesis was not affected by caudal elevation in most rats in which the inguinal canal was ligated or in rats elevated by whole-body harness. Concentrations of testosterone in serum and testicular interstitial fluid were lower (P less than 0.05) in suspended rats, regardless of the method used for caudal elevation or anatomic location of testes. Concentrations of luteinizing hormone in serum were elevated (P less than 0.05) in rats with intra-abdominal testes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗