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Biomedical subjects

S L Lightman

Publications and source records attributed to S L Lightman.

At least 433 records · Page 24Linked to original sources
PubMed1981

The diagnosis of primary hyperaldosteronism.

An aldosterone-suppression test based on a simple method of extracellular-fluid volume expansion over three days reliably discriminated between patients with aldosterone-producing adenomas, idiopathic adrenal hyperplasia, and essential benign hypertension. In patients with primary hyperaldosteronism adrenal-vein plasma aldosterone/cortisol concentration ratios successfully lateralised all 21 adenomas. In patients with an adenoma the contralateral adrenal gland was always suppressed, as indicated by a ratio which was less than that seen in the lower inferior vena cava, whereas in patients with hyperplasia the adrenal-vein aldosterone/cortisol concentration ratio from each adrenal was always greater than that seen in the lower inferior vena cava. Thus adrenal-vein sampling not only lateralises solitary adenomas but also discriminates between patients with an adenoma or hyperplasia. However, in view of the diagnostic reliability of the suppression test, it is suggested that adrenal-vein sampling is unnecessary in hyperaldosteronism due to adrenal hyperplasia.

Adenoma↗
PubMed1981

Studies of diurnal changes in plasma renin activity, and plasma noradrenaline, aldosterone and cortisol concentrations in man.

Diurnal studies were performed on ten normal volunteers taking a normal sodium diet. Half-hourly blood samples were taken throughout 25 h and assayed for plasma renin activity (PRA) and the plasma concentrations of noradrenaline, aldosterone and cortisol. Sleep was recorded polygraphically and scored by standard criteria. Circadian rhythms were demonstrated for plasma cortisol, aldosterone and noradrenaline concentrations, but not for plasma renin activity. The nadir of the rhythm for the noradrenaline concentration appeared to be related to sleep itself rather than to any chronological index. Only PRA was effected by the stage of sleep, falling sharply during periods of REM sleep. Plasma cortisol and aldosterone concentrations showed a positive correlation over the 24 h. There was, however, no correlation between PRA and plasma aldosterone concentrations, except when the subjects arose after their night's recumbency. Plasma noradrenaline concentration did not correlate with the concentration of any of the other hormones measured.

Adult↗
PubMed1981

Failure of 2-hydroxyoestrone to lower prolactin concentrations in hyperprolactinaemic women.

The catechol oestrogen 2-hydroxyoestrone has been reported to lower serum prolactin concentrations acutely in normal women and it has been proposed that it may be effective in suppressing prolactin secretion in hyperprolactinaemic patients. Five women with hyperprolactinaemia and anovulation were studied. Following a control infusion, 2-hydroxyoestrone was given at a rate of 80 micrograms/h for 4 h. In no patient was there a fall in prolactin levels and no changes were observed in gonadotrophin concentrations. We conclude that a short-term infusion of 2-hydroxyoestrone, at a dose which will produce high blood levels of the steroid, does not affect prolactin or gonadotrophin secretion in hyperprolactinaemic states.

Adult↗
PubMed1981

Studies on the responses of plasma renin activity and aldosterone and cortisol levels to dopaminergic and opiate stimuli in man.

Evidence for a role of dopamine and endogenous opioids in the control of the secretion of renin and adrenal steroids was sought in man. The effects of L-dopa, L-dopa plus carbidopa, dopamine, domperidone and naloxone were studied on the renin and aldosterone responses to head-up tilt. L-dopa diminished the rise in renin following tilt and this effect of L-dopa was abolished by carbidopa. Aldosterone was not significantly affected by any of the compounds. Cortisol secretion was stimulated by carbidopa plus L-dopa more than L-dopa alone, and was also increased by both dopamine and naloxone. The significance of these findings is discussed.

Adult↗
PubMed1981

Climacteric flushing: clinical and endocrine response to infusion of naloxone.

Six postmenopausal women with frequent attacks of flushing were studied by measuring plasma luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin and noradrenaline concentrations at regular and frequent intervals and at the time of each of 82 flushes. The hormone measurements were made on a control day and on the second day during infusion of either naloxone (22 micrograms/min) or saline. The perception of a flush was associated with a significant increase of plasma LH concentrations. There were no significant changes in plasma FSH, prolactin or noradrenaline concentrations. Naloxone infusion resulted in a highly significant reduction in the frequency of flushes and in the number of LH pulses. We conclude that flushing and its neuro-endocrine correlates are related to activation of opiate receptors. Naloxone may provide the basis for a non-steroidal treatment of climacteric flushing attacks.

Adult↗
PubMed1981

Constancy of opioid control of luteinizing hormone in different pathophysiological states.

This study assessed the effect of the opiate antagonist naloxone on anterior pituitary hormone release in normal subjects and patients with disturbances of the gonadotropic axis. Intravenous bolus injections of naloxone resulted in a rise of plasma LH, but had no significant effect on plasma levels of FSH or PRL. It also failed to alter the LH, FSH, or TSH response to LRF and TRH, although it did augment the PRL response to TRH. Slow iv infusion of naloxone resulted in increased plasma LH and FSH concentrations in both normal subjects and patients with hyperprolactinemia. The rise of LH correlated with the mean basal LH concentrations; a low basal level only responded to naloxone with a small increase in circulating LH concentration and vice versa. This relationship of the response of LH to the resting levels also held in several other pathological states in which there were marked differences of androgen and estrogen status as well as up to a 100-fold variation in basal LH concentrations. It is concluded that LH is under inhibitory opioid control both in normal subjects and in widely differing pathological states of the gonadotropic axis.

Adenoma↗
PubMed1980

Evidence for dopamine as an inhibitor of vasoprotein release in man.

The effect of dopamine on vasopressin release was studied by the infusion of L-Dopa, a dopamine precursor that crosses the blood-brain barrier. L-Dopa suppressed resting levels of vasopressin and inhibited the rise of vasopressin produced by head-up tilt. Carbidopa, a decarboxylase inhibitor that does not cross the blood-brain barrier blocked the action of L-Dopa. These results suggest that dopamine inhibits the release of vasopressin, either by an action at pituitary level or at the median eminence of the hypothalamus.

Adult↗
PubMed1980

A relationship between plasma renin activity and the rapid eye movement phase of sleep in man.

The possible influence of the central nervous system on renin release was investigated by simultaneously monitoring the PRA and the changes of the sleep-wake cycle. Nine normal volunteers were studied, 2 of whom were subjected to an acute sleep reversal procedure. PRA exhibited marked intra- and intersubject variability. No consistent diurnal or ultradian rhythm was observed. The nocturnal variation in PRA, however, was associated with changes in the stage of sleep. The rapid eye movement (REM) phase correlated with a decrease in PRA. In the 9 subjects, 26 measurements were made during REM, all but 2 of which showed a drop compared to the level obtained in the immediately preceding sleep stage (P less than 0.001), by two-tailed t test). The mean decrease in PRA accompanying REM was 407 pg/ml.h, and the mean time for PRA to decrease by half after REM onset was 33 min, with a SE of 8 min. The sleep reversal procedure confirmed that REM was associated with decreased PRA even when sleep occurred at an unaccustomed time. REM is demonstrated by these findings to be temporally associated with a suppression of PRA. The rate of decrease of PRA after REM onset closely approximates the most recent estimations of PRA half-life, which suggests that REM onset is associated with a virtual cessation in renin production.

Adult↗
PubMed1980

Evidence for endogenous opioid control of vasopressin release in man.

The role of endogenous opioids in the control of vasopressin secretion was studied using the pure opiate antagonist naloxone. Naloxone both reduced resting levels of vasopressin and inhibited the rise in vasopressin induced by an orthostatic stimulus. These results suggest that endogenous opioids are important as a tonic stimulus to vasopressin release in man.

Adult↗
PubMed1980

Effects of the opiate antagonist naloxone and the enkephalin analog DAMME on the vasopressin response to a hypertonic stimulus in man.

Experiments were performed to study the effects of opioids on both the plasma arginine vasopressin and renal responses to hypertonic saline. Neither the opiate antagonist naloxone nor the enkephalin agonist DAMME [D-Ala2, MePhe4, Met (0)-ol)enkephalin] altered the vasopressin response to the same hypertonic stimulus, although DAMME increased free water clearance. In man, opioids do not seem to be important mediators of the vasopressin response to osmolar change.

Adult↗
PubMed1980

Refractory oedema.

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Aminophylline↗
PubMed1979

Distribution of beta-endorphin in normal and schizophrenic human brains.

beta-Endorphin was measured by radioimmunoassay in post-mortem human brains. Samples of brain were taken from five discrete areas, both from control brains and brains of schizophrenic patients. No difference in beta-endorphin levels was found in these two groups of brains. beta-Endorphin was confirmed to be widely distributed in the brain, but there were considerable differences in the concentrations in different areas.

Brain Chemistry↗
PubMed1978

Phenobarbital dyskinesia.

A patient was admitted to hospital following an overdose of phenobarbital. During her recovery she developed both chorea and torsion dystonia which could only be related to her high plasma phenobarbital levels.

Adult↗