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Biomedical subjects

S Kapen

Publications and source records attributed to S Kapen.

At least 19 recordsLinked to original sources
PubMed1987

The cardioacceleratory response to arecoline infusion during sleep in narcoleptic subjects and controls.

Nine narcoleptic and nine control subjects underwent 4 nights of sleep recordings. On nights 3 and 4, they received continuous intravenous infusions of saline. Additionally, on both nights they received 0.2 mg glycopyrrolate at the end of the first REM period (REM1) and 0.5 mg arecoline or placebo in random order 20 min after the end of REM1. Heart rates were counted for a 40-min period following the end of REM1. There was a significant and similar cardioacceleratory effect after arecoline in both narcoleptic and normal subjects, beginning at 5 min from the start of the infusion and peaking at 9 min. Placebo had no effect. Narcoleptic subjects had consistently higher baseline heart rates than controls on infusion and noninfusion nights, most likely owing to age differences between the two groups. The results suggest that narcoleptic persons do not have increased cholinergic sensitivity, or that the canine model of narcolepsy differs from the human model, or that the muscarinic receptors that play a role in the pathophysiology of narcolepsy differ in sensitivity from those that regulate heart rate.

Adult↗
PubMed1987

Bimodality electrophysiologic evaluation of brainstem in sleep apnea syndrome.

Previous electrophysiologic studies in the sleep apnea syndrome (SAS) have used only a single modality (brainstem auditory evoked responses [BAERs]) and yielded conflicting, inconsistent, and inconclusive results. We utilized both BAERs and somatosensory evoked responses in 12 patients with SAS and found normal central conduction times in all patients. These data argue against a significant structural alteration in both rostral and caudal brainstem, insofar as the auditory and somatosensory pathways are concerned, in patients with SAS.

Adult↗
PubMed1986

Cholinergic enhancement and REM sleep latency in the aged: lecithin does not reproduce physostigmine effect.

The administration of lecithin has failed to improve memory in aged or demented individuals. We studied the effect of lecithin on another cholinergic function, REM sleep latency. Intravenous doses of physostigmine shortened the latency to the first REM sleep period, but oral lecithin did not. In contrast to physostigmine, brain cholinergic function may not be enhanced by lecithin, which may explain why lecithin does not improve cognitive function.

Acetylcholine↗
PubMed1981

A "pubertal" 24-hour luteinizing hormone (LH) secretory pattern following weight loss in the absence of anorexia nervosa.

A 32-year-old women with no evidence of anorexia nervosa lost 20 pounds following a self-imposed diet and developed secondary amenorrhea. On two separate occasions, 24-hour plasma sampling at 20-minute intervals the monitoring of nocturnal sleep revealed a "pubertal" pattern of luteinizing hormone (LH) secretion, i.e., sleep-related enhancement of LH. After she regained 15 pounds, the "pubertal" pattern reverted to the typical of adults in which there is no significant difference in LH secretion between average sleep and waking values. One month following the last study, normal menses began. These data demonstrate that weight loss or the metabolic factors associated with nutritional changes, in the absence of anorexia nervosa, may be associated with amenorrhea and reversion to the "pubertal" pattern of LH secretion, which can return to normal following weight gain.

Adult↗
PubMed1980

Failure of a serotonergic receptor-blocking drug to change the twenty-four-hour luteinizing hormone secretory pattern in women.

The 24-h LH secretory pattern in women during the early follicular phase is characterized by inhibition during the early sleep period. Methysergide maleate was administered to six normal women to test the hypothesis that the effect of sleep on LH secretion is due to serotonergic mechanisms. The results demonstrated no change in the sleep effect on LH secretion after drug administration. The 4-h average deviation after sleep onset from the 24-h mean was -27.7% for the control studies and -25.5% after methysergide maleate. The data suggest tht serotonergic pathways are not critically involved in the control of the 24-h LH secretory program in women.

Adult↗
PubMed1978

Twenty-four-hour plasma prolactin patterns in prepubertal and adolescent boys.

The concentration of PRL was measured every 20 min for 24 h in six prepubertal and three adolescent boys. In both groups, PRL secretory episodes occurred throughout the 24-h period. In all subjects, the mean concentration of PRL was significantly higher during sleep than during wakefulness; the mean concentration during the entire 24-h period, during sleep or during wakefulness, was not different between the prepubertal subjects and the adolescents. These data suggest the absence of an ontogenetic change for PRL secretion in boys. During acute sleep-wake reversal, two of three pubertal boys showed significantly higher PRL during daytime sleep than during nocturnal wakefulness. This suggest that PRL release in adolescent boys is linked with sleep, rather than with clock time.

Adolescent↗
PubMed1976

The relationship of luteinizing hormone secretion to sleep in women during the early follicular phase: effects of sleep reversal and a prolonged three-hour sleep-wake schedule.

The relationship of luteinizing hormone (LH) secretion to sleep in adult women was investigated in two ways: an acute 180 degrees sleep-wake cycle reversal in a group of six women and a schedule in which a young woman engaged in a three hour sleep-wake cycle (two hours awake, one hour allowed for sleep continuously for ten days--the study was carried out on the eighth day). Each subject in the reversal study had a baseline period during which plasma samples were collected every twenty minutes for twenty-four hours and nocturnal sleep was monitored electrophysiologically during the early follicular phase of the menstrual cycle. During a succeeding cycle, the study was repeated after sleep-wake reversal. LH secretory patterns were analyzed by comparing the 24-hour mean plasma LH concentration with the hourly averages in percentage terms, using Stage 2 sleep onset as the zero point. LH secretion was depressed to approximately the same degree in both the baseline and reversal studies. The average hourly percentage difference from the 24-hour mean for the four-hour period following sleep onset was -13.4% and -13.1% for the baseline and reversal, respectively. These percentage deviations represented practically the entire negative deviation for the 24-hour period in both studies. The difference between the first four-hour period after sleep onset and the second was significant. The subject on a three-hour cycle had a baseline in which a large decrease in LH secretion occurred after sleep onset (-52.2% during the third hour). Her LH secretory pattern during the three-hour sleep-wake schedule was characterized by a fall during sleep periods, particularly when slow wave sleep (SWS) predominated. However, no correlation was found between specific sleep stages and LH secretion in the six women of the reversal study. These results confirm a relationship of LH secretion to sleep in adult women, one which is different from that described during puberty.

Adult↗
PubMed1976

Clinical and laboratory heterogeneity in idiopathic hypogonadotropic hypogonadism.

Six young men with idiopathic hypogonadotropic hypogonadism had 24-h frequent blood sampling studies for measurement of LH, FSH and testosterone. Five of the patients had LH and FSH measured after administration of 100 mug LH-RH during waking and then during sleep. Four of the patients had testicular biopsies performed. The results of the present studies showed that 4 of the patients had no evidence of episodic LH, FSH, or testosterone secretion. The two patients who showed significant sleep related pulses of LH had the highest 24 h mean testosterone concentrations, the best responses to exogenous LH-RH and the most differentiated testicular biopsies. Sleep had no effect on the release of LH or FSH in response to LH-RH. These sutdies suggest that the clinical and laboratory heterogeneity of idiopathic hypogonadotropic hypogonadism may be the result of differences in the degree of endogenous LH-RH deficiency.

Adult↗
PubMed1976

Human puberty: 24-hour estradiol in pubertal girls.

Plasma luteinizing hormone, follicle-stimulating hormone, and estradiol were measured at 20-minute intervals for 24-hours in seven pubertal premenarchal girls whose sleep was monitored polygraphically. A circadian variation in plasma estradiol was demonstrated with the highest values occurring during the day (1400-1600 hours) and lowest values during sleep, a time when gonadotropin secretion was augmented.

Adolescent↗
PubMed1975

Twenty-four-hour secretory patterns of gonadotropins and prolactin in a case of Chiari-Frommel syndrome.

Plasma LH, FSH and prolactin secretory patterns were derived from the measurement of 20-min interval plasma samples obtained during a complete 24-h period in a patient with persistent postpartum amenorrhea and galactorrhea (Chiari-Frommel syndrome), before and after clomiphene citrate therapy. During nocturnal sleep, polygraphic monitoring was carried out to precisely identify sleep onset, specific sleep stages and waking periods. During the evening and nighttime hours, LH and FSH concentrations were markedly reduced, compared to the daytime patterns both before and after clomiphene therapy. A sleep associated rise of prolactin concentration was present, similar to the pattern found in normal subjects but at higher concentrations. The reciprocal nature of the nocturnal secretory patterns for LH and FSH and prolactin in this patient suggests an alteration in hypothalamic dopaminergic mechanisms which are thougt to control the secretion of these hormones.

Adult↗
PubMed1975

Twenty-four hour prolactin (PRL) secretory patterns during pregnancy.

To determine if the central nervous system "program" controlling PRL secretion is operative during pregnancy, three pregnant women (12th, 20th and 32nd week of gestation) had 24-hour, 20-minute interval plasma sampling and polygraphic monitoring of nocturnal sleep. All three subjects showed episodic PRL secretion during waking which became augmented during nocturnal sleep. Since the number of "major" PRL secretory episodes was similar to normals, the increased PRL levels were most probably achieved by increased secretion per secretory episode. These findings suggest that during pregnancy, the PRL sleep related secretory "program" is maintained in a qualitative manner, albeit at a higher set-point.

Adult↗
PubMed1974

Hypothalamic-pituitary function in diverse hyperprolactinemic states.

Prolactin secretion in normal adults is characterized by periods of episodic secretion which increase in magnitude during sleep. In this study, we report the 24-h mean prolactin concentrations, prolactin secretory patterns, and associated pituitary hormone function in nine patients (seven women and two men) with hyperprolactinemia of diverse etiologies. Four of the women and one of the men had clinically demonstrable pituitary tumors, one boy had a hypothalamic tumor, and the three other women had "functional" hyperprolactinemia. The 24-h mean prolactin concentrations derived from averaging the 20-min interval samples for 24 h ranged from 28.6 to 1,220 ng/ml. The plasma prolactin patterns in these patients showed persistence of episodic secretion in all and loss of the normal sleep-wake difference in plasma prolactin in seven of nine. Three of the patients with galactorrhea and comparable 24-h mean prolactin concentrations (58.3, 59.7, and 64.3 ng/ml) showed similar prolactin secretory patterns despite different etiologic mechanisms. Evaluation of the secretory patterns of luteinizing hormone (LH) in these patients showed loss of normal pulsatile LH release and a low 24-h mean LH concentration in the patient with the pituitary tumor, while the two patients without clinically demonstrable pituitary tumors ("post-pill" galactorrhea and "idiopathic" galactorrhea) showed normal LH secretory patterns and 24-h mean LH concentrations. The 24-h mean cortisol concentrations and secretory patterns were normal in five of the seven patients who had these parameters measured. The patient with the hypothalamic tumor had a low 24-h mean cortisol concentration and production rate and absent response to metyrapone. The patient with "idiopathic" galactorrhea had an elevated 24-h mean cortisol concentration but normal cortisol production rate and urinary 17-hydroxycorticoid excretion. Growth hormone secretion was abnormal in four of the patients (one with the hypothalamic tumor and three with pituitary tumors). Thyrotropin-releasing hormone (TRH) administration in four patients resulted in normal TSH release in two patients (one of whom developed galactorrhea after the test), an absent response in the patient with the hypothalamic tumor, and a blunted response in one of the women with a pituitary tumor. The two men had low 24-h mean plasma testosterone concentrations (69 and 30 ng/100 ml) and symptoms of impotence and loss of libido. Five of the women (four with pituitary tumors and one with Chiari-Frommel syndrome) had either low 24-h mean LH concentrations, abnormal LH secretory patterns, or both. These data indicate that patients with hyperprolactinemia encompassing a varied etiological range frequently show loss of the normal sleep-associated increase in prolactin secretion as well as abnormalities in the regulation of the other hypothalamic pituitary-regulated hormones. The finding that the abnormalities in LH, growth hormone, thyrotropin, and cortisol (adrenocorticotrophic) secretion were almost uniformly confined to the patients with the clinically demonstrable hypothalamic or pituitary tumors suggests that the size of the lesion is the critical factor.

17-Hydroxycorticosteroids↗