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Biomedical subjects

W B Mendelson

Publications and source records attributed to W B Mendelson.

At least 145 records · Page 8Linked to original sources
PubMed1979

Neuroendocrine effects of haloperidol in an adolescent with Gilles de la Tourette's disease and delayed onset of puberty.

The effects of haloperidol on the release of prolactin, growth hormone, and luteinizing hormone during sleep were studied in an adolescent male who had Gilles de la Tourette's disease and delayed onset of puberty. At doses of 5 and 2 mg, haloperidol led to an increase of prolactin secretion and a suppression of luteinizing hormone release. Growth hormone was unaffected. Despite these changes, the patient had normal secondary sexual development consistent with puberty.

Adolescent↗
PubMed1978

Physostigmine alters onset but not duration of REM sleep in man.

Physostigmine (1.0mg) or placebo were administered intravenously over 1-h period to seven male normal volunteers beginning 35 min after sleep onset. The results indicate that physostigmine induced the onset of REM sleep but did not significantly alter the duration of individual REM sleep periods. Physostigmine significantly shortened the REM latency and the duration of the second nonREM period. After inducing the onset of the first REM period(s); physostigmine also appeared to advance succeeding REM-nonREM sleep cycles relative to sleep onset even when the duration of each cycle was unaffected.

Adult↗
PubMed1978

Effects of the acute administration of ethanol on the sleep of the rat: a dose-response study.

Seven-hr sleep recordings were performed on rats following intraperitoneal injection of saline or one of four doses of ethanol (1.1, 1.5, 2.0 or 2.5 g/kg). Total minutes of REM sleep and percentage REM sleep were decreased in a dose-dependent manner. Percentage nonREM sleep increased with progressively higher doses. The decrease in REM sleep appeared to be related to a decrease in the number of REM sleep episodes and an increase in the length of the REM-nonREM cycle. Other variables such as mean length of REM sleep episodes and REM sleep efficiency were unchanged. An analysis of the first and second 3.5 hr of the recording showed that ethanol continued to have marked effects on REM and nonREM sleep during the second 3.5 hr, when blood levels were declining. Ethanol produced decreases in sleep latency, but total sleep time was unchanged.

Animals↗
PubMed1978

Methoscopolamine inhibition of sleep-related growth hormone secretion. Evidence for a cholinergic secretory mechanism.

We have examined the effects of cholinergic blockade with 0.5 mg methscopolamine bromide, intramuscularly, on sleep-related and insulin-induced growth hormone (GH) secretion. 17 normal young men were studied; 8 had sleep studies, and 12 (including 3 who also had sleep studies) had insulin tolerance tests (ITT) with 0.1 U/kg of regular insulin. After an adjustment night in the sleep laboratory, saline control night and methscopolamine night studies were done in random sequence; study procedures included electroencephalographic, electromyographic, and electrooculographic recordings, and blood sampling every 20 min for hormone radioimmunoassays. Prolactin levels were also measured during sleep. For methscopolamine night studies, the mean overall control GH level of 2.89+/-0.44 ng/ml and the mean peak control GH level of 11.09+/-3.11 ng/ml were dramatically reduced to 0.75+/-0.01 and 1.04+/-0.25 ng/ml, respectively (P<0.0001 and <0.001). Despite virtual absence of GH secretion during the night in every study subject, no measured sleep characteristic was affected by methscopolamine, including total slow-wave sleep (12.1+/-2.6% control vs. 10.3+/-2.5% drug, P>0.2). Sleep prolactin levels were not changed by methscopolamine. In contrast to the abolition of sleep-related GH secretion, administration of methscopolamine had only a marginal effect on the GH response to insulin hypoglycemia. None of nine time points differed significantly, as was also the case with peak levels, mean increments, and areas under the curves (P>0.2). Analysis of variance did, however, indicate that the lower GH concentrations achieved during ITT after methscopolamine (average 31.7% below control) were significantly different than control concentrations. We conclude that the burst of GH secretion which normally occurs after sleep onset is primed by a cholinergic mechanism which does not influence slow-wave sleep. Cholinergic mechanisms do not appear to play an important role in sleep-related prolactin secretion. The contrast between the complete suppression of sleep-related GH release and the relatively small inhibitory effect on ITT-induced GH secretion suggests that the neurotransmitter mechanisms, and presumably the pathways, which subserve sleep-related GH secretion in man may be different from those which mediate the GH response to pharmacologic stimuli such as insulin.

Adult↗
PubMed1978

Failure of nocturnal prolactin suppression by methysergide to entrain changes in testosterone in normal men.

In order to investigate further the postulated relationship between the secretion of PRL and testosterone, 10 normal young men were studied during polygraphically recorded sleep. Concentrations of LH and testosterone were measured in plasma every 20 min, and the results were analyzed in relation to sleep parameters and previously reported (J Clin Invest 56: 690, 1975) concentrations of PRL. All subjects were studied on a control night after placebo administration and on an experimental night after ingestion of the serotonin receptor blocker, methysergide. Analysis of variance revealed that concentrations of testosterone rose gradually during sleep on both nights, as has been noted in previous studies. Highest LH values occurred during stage 1 sleep, but were only 25% higher than the lowest values, which were seen in stage 4. As shown previously, PRL concentrations were markedly suppressed by methysergide treatment. However, no significant change in testosterone values were observed on the methysergide nights as compared to the control nights. When the data were analyzed by a correlational approach, again, no significant relation between concentrations of PRL and testosterone was found. Although these data do not support the concept that PRL-stimulated testosterone secretion occurs during the night in normal men, this study does not rule out the possibility that such a mechanism may be operative during daytime hours, or under conditions of PRL stimulation rather than PRL suppression.

Humans↗
PubMed1978

Sleep during chronic ethanol administration and withdrawal in rats.

After a priming dose, ethanol was administered at a rate relative to behavioral impairment for 4 days and its effects on sleep were monitored by EEG. EEG's during withdrawal indicated an initial sleep loss followed by a return of total sleep and a REM sleep rebound several days later.

Alcoholic Intoxication↗
PubMed1977

Cocaine effects on sleep parameters in the rat.

Cocaine in 6 mg/kg doses was administered orally and intraperitoneally to rats and sleep EEG's recorded. Cocaine significantly reduced total sleep time, slow-wave sleep, and sleep latency. Rapid eye movement sleep (REM) was significantly suppressed during the first half of the sleep recording. These effects were evident by both routes of administration. The effects of cocaine on total sleep time in animals parallels that observed in man.

Administration, Oral↗
PubMed1977

A method for sleep depriving rats.

A method is described for sleep depriving up to 12 rats at a time by placing them in two large rotating cylinders. EEG data, previously unavailable for rats treated in this manner, show that total sleep time was significantly reduced from 47.0% to 3.8% of a 24-hr period. There was no selective reduction of REM or non-REM sleep.

Animals↗
PubMed1976

Polydipsia, hyponatremia, and seizures in psychotic patients.

Case histories are presented for four psychotic patients who ingested large quantities of water and subsequently developed grand mal seizures and serum sodium levels of less than 121 meq/liter. The physiology of psychogenic polydipsia and related disorders is reviewed. The relation of this disorder to temporal lobe seizures and to the use of phenothiazines is considered.

Adult↗