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Biomedical subjects

D M Lawson

Publications and source records attributed to D M Lawson.

At least 91 records · Page 5Linked to original sources
PubMed1977

The influence of long term estrogen treatment on plasma prolactin levels induced by ether anesthesia in ovariectomized rats.

2 methods of continuous estrogen delivery, polyestradiol phosphate injection and implantation of Silastic capsules of estradiol-17 beta, in ovariectomized rats induced increases in plasma prolactin in the afternoon (15.00-17.00) beginning at 1 week and continuing for 4-8 weeks. In addition these methods of estrogen treatment potentiated the ether-induced increase in plasma prolactin in the morning (9.00-11.00) beginning on week 2 and continuing for 3-8 weeks. These results indicate that estrogen activates the mechanisms that cause an afternoon surge in prolactin before potentiating a morning elevation induced by ether anesthesia.

Anesthesia↗
PubMed1977

The dipsogenic effect of alcohol and the loss of control phenomenon.

A counterbalanced within-subjects design was employed to assess the acute effects of alcohol ingestion on thirst and fluid intake and to relate these effects to the dehydration known to result from acute ingestion of alcohol. Fourteen male nonalcoholic social drinkers between the ages of 18 and 30 consumed 0.8 gm of alcohol/kg body weight during one experimental session and a placebo (0.05 gm/kg) of equal volume during the other. During the 90-minute drinking period and for one hour both before and afterward, urine specimens were collected. After the drinking period, blood alcohol levels and unobstrusive measures of ad lib drinking were recorded. In addition, subjects rated their degree of thirst three times during each session. Analyses of variance indicated that alcohol significantly increased both fluid intake and urine output, and decreased urine specific gravity. Moreover, thirst ratings were also significantly greater after alcohol than after placebo and fluid intake after alcohol was significantly correlated with prior measures of fluid balance, mean urine specific gravity, peak blood alcohol level and thirst. The implications of these results for the loss of control in alcoholism are discussed and a new theoretical account of the phenomenon is proposed.

Adult↗
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

The interaction of dopaminergic and serotonergic drugs on plasma prolactin in ovariectomized, estrogen-treated rats.

Pharmacologic agents that either block or stimulate dopaminergic or block serotonergic receptors were administered intraarterially alone or in combination to ovariectomized, estrogen-treated rats. Prolactin was estimated by radioimmunoassay of plasma collected by serial blood sampling from chronic aortic catheters. Apomorphine (10 mg/kg) depressed, whereas Pimozide (50 and 250 mug/kg) and Methiothepin (50, 500 and 5000 mug/kg) markedly increased prolactin levels. Apomorphine completely blocked the increases induced by the lowest does of Pimozide and Methiothepin, as well as the initial increases at the higher doses. However, at later time intervals after large doses of Pimozide and Methiothepin in apomorphine-pretreated rats there was a marked rebound of prolactin which was greater than the level induced by each drug alone. The serotonin antagonists SQ 10,631 and methysergide reduced the Pimozide-induced elevation in prolactin levels, suggesting that part of the increase in prolactin following dopaminergic blockage may result from the action of a tonically stimulatory serotonin system that is normally masked by the intense tonic inhibition by the dopaminergic system.

Animals↗
PubMed1975

The influence of adrenergic, dopaminergic, cholinergic and serotoninergic drugs on plasma prolactin levels in ovariectomized, estrogen-treated rats.

Levels of plasma prolactin were estimated in ovariectomized, estrogen-treated rats following the systemic administration of several neural blocking and stimulating drugs. Phenoxybenzamine, an alpha-adrenergic blocker, at high doses, increased plasma prolactin. Phenotlamine, another alpha-adrenergic blocker, and propranolol, a beta-adrenergic blocker, also increased prolactin but the responses were small and transient. Clonidine, an alpha-adrenergic stimulating drug, elevated prolactin levels whereas the beta-adrenergic stimulator isoproterenol had no effect. Dopaminergic blockade by pimozide increased levels of prolactin while stimulation of dopamine receptors by apomorphine decreased prolactin release. Atropine (a muscarinic chilinergic blocker), arecoline (a muscarinic stimulator) and nicotine (a nicotinic cholinergic stimulating drug) did not affect basal prolactin levels. Mecamylamine (a nicotinic blocker) produced a small transient elevation in plasma prolactin. Methiothepin, an alleged serotoninergic blocker, markedly increased prolactin secretion, as did serotonin. The data suggested the involvement of several neurotransmitters in the control of basal secretion of prolactin.

Adrenergic alpha-Antagonists↗
PubMed1975

Influence of anaesthetics on basal, perphenazine-induced and thyrotrophin releasing hormone-induced prolactin secretion in ovariectomized, oestrogen-treated rats.

Plasma levels of prolactin were determined, by radioimmunoassay, in ovariectomized, oestrogen-treated rats after administration of ether, sodium pentobarbitone, urethane, chloral hydrate or ketamine. These anaesthetics, when administered alone, induced sustained increases in the plasma level of prolactin (continuous ether inhalation), no change in prolactin secretion (urethane), or depressions in the level of prolactin (sodium pentobarbitone, chloral hydrate and ketamine). These same anaesthetics when given before perphenazine failed to alter the stimulatory effect of this phenothiazide on prolactin secretion. Sodium pentobarbitone did not alter the normal increase in prolactin concentration after intra-arterial administration of synthetic thyrotrophin releasing hormone (TRH). These results indicated that anaesthetics do not affect the response of either the central nervous system or the anterior pituitary to perphenazine or TRH although they affect prolactin secretion when administered alone. The site of action of anaesthetics must, therefore, be different from that of perphenazine or perphenazine must be capable of overcoming their influence by direct action on the pituitary.

Anesthetics↗