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Biomedical subjects

M G Subramanian

Publications and source records attributed to M G Subramanian.

At least 73 records · Page 4Linked to original sources
PubMed1977

Lack of a circannual cycle of daytime serum prolactin in man and monkey.

Serum samples were obtained from 7 subjects (6 men and 1 woman) in the morning (09.00 h) and in the afternoon (15.00 h) of each week for a period of 13 months and assayed for prolactin by RIA. In addition, 4 female monkeys were sampled once weekly in the afternoon for approximately two years. The data were analyzed for cyclicity by power spectrum analysis. In both species a serum prolactin circannual cycle was not obvious. In most subjects statistically significant (P less than 0.05) cycles were observed; however, there was considerable variability among individuals in the duration of the cycle, which ranged between 4 and 50 weeks. A similar result was also observed for the monkey data; here the cycles ranged between 7 and 51 weeks. The physiologic significance of these cycles is unknown at present. It is suggested that although there appears to be no diurnal serum prolactin circannual cycle, this does not rule out the possibility that there may be a nocturnal circannual cycle.

Adult↗
PubMed1976

Further studies on the effects of adrenergic, serotonergic and cholinergic drugs on the afternoon surge of plasma prolactin in ovariectomized, estrogen-treated rats.

The involvement of adrenergic, serotonergic and cholinergic mechanisms in the diurnal surge of plasma prolactin (Prl) secretion has been examined using ovariectomized, polyestradiol phosphate-treated (PEP) rats bearing aortic catheters. An afternoon surge in plasma Prl was observed to peak at 15.00 h and 17.00 h followed by declining levels at 19.00 and 21.00 h. This pattern was observed between 5 and 21 days after PEP administration. The alpha-adrenergic blocker, phenoxybenzamine (Phenox), completely prevented the Prl surge. The beta-blocker, propranolol (Propra), appeared to delay the onset and intensity of the diurnal Prl surge so that maximum levels were observed at 19.00 and 21.00 h. The serotonergic blocker, methysergide (MES), delayed the maximum diurnal Prl level until 21.00 h, while cyproheptadine (Cypro), another serotonergic blocker, significantly inhibited the surge. The muscarinic cholinergic agonist, arecoline (Arec), when administered at 12.00 h, delayed the surge, while the repeated administration of Arec completely blocked the surge. Atropine (Atro) (10 m/kg at 12.00 h and 5 mg/kg every 2 h thereafter) did not have any effect on the Prl surge, but when administered simultaneously with Arec, prevented the inhibitory effect of Arec on Prl release. The data suggested that the adrenergic and serotonergic systems have a positive input in the occurrence and magnitude of the surge and that the cholinergic system does not appear to have a physiologic role in tonically inhibiting Prl release, but may function under certain special conditions.

Animals↗
PubMed1976

Influence of cholinergic receptor blockade on drug-induced prolactin release in the monkey.

The influence of varying doses of perphenazine, thyrotropin-releasing hormone (TRH) and serotonin on prolactin release was examined in two species of monkeys: rhesus (Macaca mulatta) and crab-eating (Macaca fascicularis). The intravenous administration of 0.33 mg/kg body weight of perphenazine or 1.0 mug/kg body weight of TRH gave a greater release of prolactin than higher doses of perphenazine (1.0 mg/kg) or TRH) (3.4 mug/kg), respectively. Prolactin release induced by serotonin at doses of 1, 5 and 10 mug/kg was similar. Both atropine sulfate (Atr-SO4) and atropine methyl nitrate (Atr-MN) at a similar base level potentiated the prolactin releasing action of the high dose of perphenazine suggesting that high doses of perphenazine activate a cholinergic inhibitory component present in the pituitary. Atropine sulfate had no potentiating action on the TRH-induced prolactin release, while Atr-MN appeared to prolong the response of TRH without potentiating it. Neither form of atropine had any influence on serotonin-induced prolactin release. The data indicated that the lower prolactin response to high doses of perphenazine and TRH were brought about by different mechanisms, and that the mechanism for perphenazine appeared to be mediated through a pituitary cholinergic system.

Animals↗
PubMed1976

The influence of cholinergic, adrenergic, and serotonergic drugs on the afternoon surge of plasma prolactin in ovariectomized, estrogen-treated rats.

The effects of systemic administration of cholinergic, adrenergic, and serotonergic drugs on the afternoon surge of plasma prolactin was investigated using ovariectomized, polyestradiol phosphate (PEP)-injected rats bearing aortic catheters. Basal prolactin levels were elevated and similar after PEP administration for a period of 5 weeks, and an afternoon surge in plasma prolactin persisted for a period of 3 weeks before the magnitude of the surge diminished. The plasma estradiol levels were significantly higher for the 1100 and 1300 h samples than for the 1500 and 1700 h samples. Cornified vaginal epithelia were predominant in the vaginal smears of all animals throughout the 49-day experimental period. The cholinergic agonists arecoline, nicotine, and carbachol significantly inhibited the afternoon surge of prolactin. The muscarinic antagonist atropine resulted in a partial inhibition of the surge while the nicotinic antagonist mecamylamine did not have any inhibitory effect. The alpha-adrenergic blockers phenoxybenzamine and phentolamine and the beta-blocker propranolol inhibited the prolactin surge, with phenoxybenzamine being most effective. The administration of the serotonergic antagonist methysergide resulted in only a partial blockade of the afternoon prolactin surge. The data suggest that both the adrenergic and serotonergic systems may have a positive input in the afternoon surge of plasma prolactin. It appears that the cholinergic system does not play a significant role in the afternoon surge.

Animals↗
PubMed1975

Anterior pituitary and plasma prolactin in rats after 2 to 90 minutes of suckling.

Separation of litter for 6 hr resulted in plasma PRL levels of 48 +/- 5.8 and 45 +/- 5.7 ng per ml and AP PRL concentrations of 6.1 +/- 0.6 and 6.3 +/- 0.5 mug per mg AP in early (4-8 days) and late (20-22 days) lactation, respectively. After a 6-hr separation period, suckling for 2, 30, 60, and 90 min resulted in highly significant increases in the plasma PRL level in early lactaiton. Increases in plasma PRL levels were not seen in late lactation except in the 30-min suckled group. In both stages of lactation the AP PRL concentrations in the suckled groups were significantly lower than in the nonsuckled groups.

Animals↗
PubMedDate not supplied

Cord blood carbohydrate-deficient transferrin levels are markedly higher than maternal.

Regular, heavy alcohol intake results in transferrin that is deficient in carbohydrate moieties. Carbohydrate-deficient transferrin (CDT) has been used as a biologic marker of heavy alcohol exposure in nonpregnant humans. There have been no reports of CDT levels in pregnancy. Our objective was to determine maternal and cord blood levels of CDT. Parturients were recruited at delivery based on graded representative alcohol consumption, from abstainers to heavy drinkers, as determined by screeners skilled at eliciting drug and alcohol histories. Maternal and cord blood serum samples were obtained at delivery. A double antibody radioimmunoassay was used to determine CDT in each sample. There were 83 paired specimens analyzed by paired t tests and stepwise regression analysis. Cord blood CDT units/liter (44.0 +/- 29.5) were significantly (P < 0.0001) higher than maternal (18.4 +/- 7.0). Maternal and cord CDT did not correlate with race, perinatal risk score, gestational age at delivery, birth weight, Apgar scores, or reported alcohol intake. Maternal CDT levels had a significant negative correlation with cigarette smoking. Cord blood CDT levels are significantly higher than maternal. While regular, heavy alcohol consumption by adults results in serum transferrin deficient in carbohydrate moieties, the reason for elevated fetal CDT is unknown.

Adolescent↗
PubMedDate not supplied

Alcohol inhibits suckling-induced prolactin release and milk yield.

The effects of acute administration of alcohol on suckling-induced prolactin (PRL) release and milk yield were studied in primiparous lactating rats. On lactation day 2, pups were culled to 8 per litter. On day 5, dams were implanted with atrial catheters. On day 10, pups were separated from the dams at 0900 hr; at 1300 hr, an extension containing heparin (50 IU/ml) and 0.9% saline was attached to the exteriorized portion of the catheter. At 1400 hr, 0.4 ml blood was removed and replaced with 0.9% saline (control) or 0.3, 0.5 or 1.0 g/kg body weight of alcohol. At 1500 hr a second blood sample was obtained followed by a second alcohol or saline infusion. Pups were returned to dams and blood samples were obtained 10, 30, and 60 min after suckling. Milk consumption was calculated by weighing pups before and after 60 min of suckling. PRL in plasma samples was measured by radioimmunoassay. Alcohol did not alter baseline serum PRL. However, suckling-induced PRL release and milk consumption by the pups were significantly inhibited. Since basal PRL was not altered following administration of alcohol, the inhibitory effect of alcohol on suckling-induced PRL release is attributed to a disruption of transmission of the impulse arising from suckling stimulus.

Animals↗
PubMedDate not supplied

Alcohol inhibition of suckling-induced prolactin release in lactating rats: threshold evaluation.

Prolactin release in response to suckling was examined in primiparous lactating rats two hours after alcohol administration. Litters were adjusted to eight pups on lactation day 2 and dams were implanted with an atrial catheter on day 6. On day 10, pups were separated from the mother at 0800 h. An extension was attached to the catheter at 1100 h. Following removal of a baseline blood sample an hour later, rats were infused with alcohol doses of 0, 0.5, 1.0, 2.0 or 2.5 g/kg body weight. Two hours later, pups were returned to dams. Subsequent blood samples were obtained 10, 30, 60, 120 and 180 min after the onset of suckling. Following 10 min of suckling, plasma prolactin for groups of rats infused with alcohol at 2.0 and 2.5 g/kg body weight were lower than control, 0.5 and 1.0 g/kg groups. The blood alcohol level (BAL) for the 2.0 g/kg group was 94 +/- 8 mg% and for the 2.5 g/kg group was 162 +/- 4 mg%. After 30 min, the BAL for the 2.5 g/kg group was 134 +/- 5 mg% and plasma prolactin was suppressed in this group compared to control, 0.5 and 1.0 g/kg groups. The BAL for the 2.0 g/kg group after 30 min of suckling was 74 +/- 9 mg% but prolactin was not significantly lower than controls. We conclude that in rats, alcohol inhibition of suckling-induced prolactin release is directly correlated to the BAL. The threshold BAL which effectively inhibits this prolactin release is lower than the human legal intoxication level.

Animals↗
PubMedDate not supplied

Alcohol effects on TRH-induced prolactin response in lactating rats: in vivo and in vitro studies.

The site of action of alcohol in inhibiting suckling-induced prolactin release in lactating rats was examined by in vivo and in vitro studies. In vivo, sulpiride- and thyrotropin-releasing hormone (TRH)-induced prolactin release was studied in lactating rats separated from their litter. On day 7, dams were implanted with an atrial catheter. On day 10, pups were removed from dams at 0800 h and, after 5 h, an extension was attached to the catheter. An hour later, a baseline blood sample was removed and was followed by sulpiride (40 micrograms/kg) administration. Additional blood samples were withdrawn over 1 h. After the 60-min sample, sulpiride-administered rats were infused with 0.0, 1.0, or 2.0 g/kg b.wt. alcohol. Following alcohol, a postinfusion blood sample was removed, TRH (4.0 micrograms/kg) was administered, and subsequent blood samples were obtained 5, 10, 20, and 30 min after TRH. For in vitro studies, cells from lactating rats in midlactation were enzymatically dissociated, plated, and on culture day 5 were exposed to 0 or 10 nM TRH. Each set of cells were additionally exposed to 0, 100, or 300 mg% alcohol and media harvested after 4 h. In a subsequent study, plated cells were exposed to increasing doses of TRH in the presence of 0, 100, or 300 mg% alcohol and media harvested as above. Prolactin in plasma (in vivo studies) and medium (in vitro studies) was measured by RIA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Effects of chronic alcohol administration on lactational performance in the rat.

Lactating rats, with litters adjusted to eight pups on day 2, were implanted with an atrial catheter on day 3 of lactation. Alcohol in doses of 0.0, 1.0, or 2.0 g/kg BW was infused from day 5 to 12. The blood alcohol levels (BALs) achieved following infusion of the initial doses were maintained for 4 hours daily by infusion. To control for the reduced food intake in alcohol administered groups, rats receiving alcohol doses of 0.0 and 1.0 g/kg BW were pairfed to 2.0 g/kg BW alcohol group. For infusion, combinations of 50% dextrose, 30% alcohol in saline and saline solutions were used for 0.0 and 1.0 g/kg BW alcohol groups whereas the 2.0 g/kg BW alcohol group received 30% alcohol in saline thereby equilizing the calorie intake of the three experimental groups. On day 12, pups were separated from the dams at 0800 h, a catheter extension was attached at 0900 h and baseline blood samples for prolactin level were taken at 1000 h. Following infusion of initial alcohol doses, samples were taken for BALs. Additional samples for BALs were removed 2 h after continuing the infusion. At the end of 4-h infusion, blood samples were taken for alcohol and postinfusion prolactin levels. In groups designed to study the suckling-induced prolactin release, pups were weighed and returned to the dams. Subsequent blood samples were taken 30 min after initiation of suckling. In nonsuckled groups, blood samples were obtained at corresponding time periods. BALs were determined by head space gas chromatography and plasma prolactin by a double antibody radioimmunoassay. Suckling latency and milk consumption during the 30 min of suckling were measured. Dams' and litter weights were determined on days 2, 5, and 12 of lactation. Infusion of alcohol for 8 days from day 5 to 12 of lactation did not affect maternal body weight. However, litters nursed by dams receiving 2.0 g/kg BW alcohol weighted less on day 12 compared to all other groups. Suckling latencies did not differ among groups. Milk consumed during the 30 min of suckling was lower for the alcohol administered groups. The inhibitory effect on milk consumption was greater for the 2.0 g/kg BW group than in the 1.0 g/kg BW alcohol group. Alcohol infusion did not affect the basal prolactin, whereas, the higher dose (2.0 g/kg BW) inhibited suckling-induced prolactin release.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Beta-endorphin-stimulated prolactin release in lactating rats following alcohol administration.

To delineate the mechanism of alcohol inhibition of the suckling-induced prolactin increase, we examined beta-endorphin-stimulated prolactin release in lactating rats separated from their litters. On day 2 of lactation litters were adjusted to eight pups. On day 7, dams were implanted with an atrial catheter; experiments were conducted on lactation day 10. Litters were separated from their dams at 0800. After five hours, a PE50 extension tube filled with heparinized saline was attached to the catheter. At 1400 a preinfusion blood sample was removed and was followed by infusion of saline (control) or alcohol in saline (1.0 and 2.0 g/kg/body weight). Following the removal of a postinfusion blood sample, beta-endorphin (600 micrograms/kg/body weight) was administered. Additional blood samples were withdrawn 10, 30, 60, and 120 min after beta-endorphin. Alcohol infusion did not alter basal prolactin. beta-Endorphin administration resulted in pronounced prolactin increases in all groups. Alcohol failed to inhibit beta-endorphin-induced plasma prolactin increase. From the present study with beta-endorphin and our previous studies with sulpiride and thyrotropin-releasing hormone (TRH) it is concluded that the anterior pituitary is not the site where alcohol acts to inhibit suckling-induced prolactin release in rats.

Animals↗