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Biomedical subjects

V Padmanabhan

Publications and source records attributed to V Padmanabhan.

At least 109 records · Page 6Linked to original sources
PubMed1984

Relationship between pituitary responsiveness to Gn-RH and number of Gn-RH-binding sites in pituitary glands of beef cows.

Changes in the ability of Gn-RH to induce gonadotrophin release with time after synchronization of oestrus was determined in 4 groups of 6 cows each. Cows were given Gn-RH at 40-min intervals for 6 h beginning at -24, 0, 18 or 36 h (time 0 = removal of progestagen implant). Changes in concentration (ng/ml) of serum LH after Gn-RH averaged 2.9, 6.2, 6.4 and 33.4, whereas serum FSH averaged 25.7, 35.8, 35.8 and 97.3. Thus the responsiveness of the pituitary to Gn-RH had increased by 36 h after implant removal. Other groups of cows subjected to the same synchronization scheme were slaughtered at 0 h, 24 h or at various times after onset of oestrous behaviour. Gn-RH binding to crude pituitary membrane preparations was assessed. There was no apparent change in the affinity constant of Gn-RH-binding sites with time after synchronization. The number of Gn-RH-binding sites remained unchanged until the period of oestrus when a significant decline with time was detected. We conclude that the increase in pituitary responsiveness to Gn-RH that occurs before the preovulatory gonadotrophin surge was not directly associated with changes in number or affinity of pituitary Gn-RH-binding sites in crude pituitary membrane preparations.

Animals↗
PubMed1983

Cortisol inhibits and adrenocorticotropin has no effect on luteinizing hormone-releasing hormone-induced release of luteinizing hormone from bovine pituitary cells in vitro.

Suckling causes a delay in onset of estrus and ovulation in cattle postpartum. In addition, the suckling stimulus causes the release of corticoids presumably via ACTH. Since any hormone released by suckling is a potential inhibitor of gonadotropin secretion and/or ovulation, we investigated the effects of ACTH and cortisol on LHRH-induced LH release from bovine pituitary cells in vitro. Anterior pituitary glands were obtained from cows killed during the luteal phase of an estrus cycle (days 5-15). Pituitary cells, disaggregated enzymatically, were grown in Dulbecco's medium containing 10% dextran charcoal-stripped fetal calf serum. On day 5, cultures were washed and reincubated in serum free medium containing the hormone being tested. After 6 h of incubation, LHRH was added in 10 microliters medium and incubation continued for an additional 6 h. ACTH at 4.3 X 10(-9), 4.3 X 10(-8), and 4.3 X 10(-7) M had no effect on basal or LHRH-induced LH release. Cortisol at 12.1 ng/ml decreased (P less than 0.001) the slope of LHRH response curve (b1 = 2.9 vs. 5.5 for controls). To determine if this effect was specific for cortisol, we compared cortisol, dexamethasone, and progesterone. LHRH-induced LH release (percent of control) was decreased (P less than 0.001) by 12.1 ng/ml cortisol (98%), 1, 5, and 10 ng/ml dexamethasone (60%, 71%, and 88%), but not by 3.1 ng/ml progesterone. The inhibitory effect of cortisol was reversible. Thus, LHRH-induced LH release (percent of controls) at 0, 24, 48, and 72 h after a 24-h exposure to 12.1 ng/ml cortisol was 19%, 89%, 100%, and 115%, respectively. We have demonstrated that cortisol at concentrations found normally in blood of cows postpartum will inhibit LHRH-induced LH release from bovine pituitary cells. This observation is consistent with the hypothesis that cortisol released by suckling may inhibit gonadotropin secretion postpartum and as such may prolong the anovulatory interval postpartum.

Adrenocorticotropic Hormone↗
PubMed1982

Estradiol induces and progesterone inhibits the preovulatory surges of luteinizing hormone and follicle-stimulating hormone in heifers.

Objectives were to determine: 1) whether estradiol, given via implants in amounts to stimulate a proestrus increase, induces preovulatory-like luteinizing hormone (LH) and follicle-stimulating hormone (FSH) surges; and 2) whether progesterone, given via infusion in amounts to simulate concentrations found in blood during the luteal phase of the estrous cycle, inhibits gonadotropin surges. All heifers were in the luteal phase of an estrous cycle when ovariectomized. Replacement therapy with estradiol and progesterone was started immediately after ovariectomy to mimic luteal phase concentrations of these steroids. Average estradiol (pg/ml) and progesterone (ng/ml) resulting from this replacement were 2.5 and 6.2 respectively; these values were similar (P greater than 0.05) to those on the day before ovariectomy (2.3 and 7.2, respectively). Nevertheless, basal concentrations of LH and FSH increased from 0.7 and 43 ng/ml before ovariectomy to 2.6 and 96 ng/ml, respectively, 24 h after ovariectomy. This may indicate that other ovarian factors are required to maintain low baselines of LH and FSH. Beginning 24 h after ovariectomy, replacement of steroids were adjusted as follows: 1) progesterone infusion was terminated and 2 additional estradiol implants were given every 12 h for 36 h (n = 5); 2) progesterone infusion was maintained and 2 additional estradiol implants were given every 12 h for 36 h (n = 3); or 3) progesterone infusion was terminated and 2 additional empty implants were given every 12 h for 36 h (n = 6). When estradiol implants were given every 12 h for 36 h, estradiol levels increased in plasma to 5 to 7 pg/ml, which resembles the increase in estradiol that occurs at proestrus. After ending progesterone infusion, levels of progesterone in plasma decreased to less than 1 ng/ml by 8 h. Preovulatory-like LH and FSH surges were induced only when progesterone infusion was stopped and additional estradiol implants were given. These surges were synchronous, occurring 61.8 +/- 0.4 h (mean +/- SE) after ending infusion of progesterone. We conclude that estradiol, at concentrations which simulate those found during proestrus, induces preovulatory-like LH and FSH surges in heifers and that progesterone, at concentrations found during the luteal phase of the estrous cycle, inhibits estradiol-induced gonadotropin surges. Furthermore, ovarian factors other than estradiol and progesterone may be required to maintain basal concentrations of LH and FSH in heifers.

Animals↗
PubMed1976

Management of preinfarction angina. Evaluation and comparison of medical versus surgical therapy in 43 patients.

Short-term results of aggressive surgical management were compared with results of medical management in forty-three patients with preinfarction angina admitted to the coronary-care unit (CCU) over an 18 month period. These patients were selected from 1,609 consecutive admissions to the CCU because they met strict criteria for preinfarction angina: severe chest pain at rest, ST-segment elevation or depression during pain which subsided rapidly after cessation of pain, and normal serum enzymes (CPK, SGOT, and LDH). Twenty-three patients had coronary angiography, done with operating room and pump standby. One patient, who had total occlusion of the left main coronary artery, died during the study. Twenty-one of the remaining patients were considered surgical candidates, and were treated immediately after angiography with 1 to 3 vein bypass grafts. There was one late postoperative death and, of the 20 survivors, 2 had ECG evidence of acute myocardial infarction and one had mild angina at time of discharge. In contrast, of the 21 patients treated medically, 13 sustained acute MI, resulting in 8 instances of congestive heart failure and 4 cases of ventricular fibrillation. Four patients died in cardiogenic shock. With the use of rigid criteria, a small subgroup of patients with variant angina at high risk of developing AMI has been identified and categorized as having preinfarction angina. Our experience suggests that aggressive surgery immediately following coronary angiography offers a lower incidence of MI, morbidity, and death than does medical management.

Aged↗