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Biomedical subjects

I Gil-Ad

Publications and source records attributed to I Gil-Ad.

At least 19 recordsLinked to original sources
PubMed1992

Platelet imipramine binding and plasma cortisol levels in Israeli civilians during the Gulf War.

[3H] Imipramine binding to platelets and plasma cortisol levels were measured in nine Israeli civilians before, during, and after repeated missile attacks. Hamilton Anxiety Rating Scale (HARS), and Beck Depression Inventory (BDI) were similar before and during the war and decreased significantly after the war. A trend toward increase in platelet imipramine binding values was observed during the war when compared with the postwar values (19%; p = 0.056), and/or when compared with prewar values (26%; p = 0.063). However, one-way analysis of variance with repeated measures did not reveal a significant statistical difference [F (2,6) = p = 2.07; NS] among the three time points. A significant correlation was found between HARS score, but not BDI, and imipramine binding values in the prewar and postwar time points (r = 0.87; 0.71, respectively). Plasma cortisol levels did not alter significantly during the study period.

Adjustment Disorders↗
PubMed1992

Growth hormone therapy in normal short children induces a transitory decrease in plasma growth hormone releasing hormone levels and in human growth hormone responsiveness to exogenous growth hormone releasing hormone.

A three-month study of the effect of growth hormone (hGH) therapy (0.1 U/kg/day sc) on plasma levels of GH releasing hormone (GHRH), somatostatin and insulin-like growth factor I (IGF-I) and on the hGH responsiveness to exogenous GHRH was carried out in 32 prepubertal short-stature children with normal GH secretion. Blood samples were collected prior to initiation of therapy, and at 5, 30 and 90 days of onset of therapy, as well as 2 and 90 days after termination of therapy. The nonconventional hGH therapy induced an increase in serum IGF-I levels which lasted as long as therapy was continued. Plasma GHRH levels showed an early transitory decrease after five days of therapy, whereas plasma somatostatin levels were unaltered. A slight suppression in hGH responsiveness to exogenous GHRH was found at 2 but not at 90 days after termination of hGH therapy. It is concluded that nonconventional hGH treatment does not cause permanent changes in physiological hGH secretion.

Adolescent↗
PubMed1992

Neuroendocrine response to trihexyphenidyl in depressed patients.

The effect of a single dose (10 mg P.O.) of trihexyphenidyl (THP) on plasma cortisol, growth hormone (GH), and immunoreactive beta-endorphin (ir-beta-EP) was studied in seven major depressed patients and seven controls. GH secretion was suppressed (34-41%) by THP in both groups. THP did not affect cortisol secretion in depressed patients and controls. An increase (18%; p less than 0.05) in plasma ir-beta-EP levels was detected in the healthy subjects only. The results of this study do not support the hypothesized altered responsiveness to anticholinergic provocation in major depression. The inhibitory activity of THP on GH secretion indicates the involvement of the cholinergic system in the regulation of GH release in humans.

Adult↗
PubMed1991

Acromegaly due to ectopic growth hormone-releasing hormone secretion by a bronchial carcinoid tumour. Dynamic hormonal responses to various stimuli.

Ectopic GHRH is a relatively uncommon cause of acromegaly, which should be differentiated from pituitary adenoma, in order to avoid damage to the pituitary gland from unnecessary interventions. We report here on a 66-year-old man with acromegaly due to a GHRH-secreting bronchial carcinoid tumour, who recovered completely following removal of the tumour. His hormonal status was studied before and after the operation. Basal GH, GHRH, IGF-I and PRL levels, as well as plasma GH response to glucose load and TRH administration were abnormal before the operation, and became normal thereafter. The somatostatin analogue SMS 201-995 was found to be a potent inhibitor of the ectopic GHRH and the GH secretion (greater than 500 to 42 ng/l and 15.4 micrograms/l to 0.8 microgram/l, respectively). The effect on GHRH proved to be due to direct effect of somatostatin on the tumour cells, as demonstrated in tissue culture studies. A mixed meal was found immediately to suppress GHRH levels without such an effect on GH secretion. We conclude that the neuroendocrine tests usually practised in acromegaly cannot differentiate between ectopic GHRH secretion and pituitary adenoma. High plasma GHRH levels may serve as a diagnostic test for excessive GHRH production, which is almost always ectopic. These high levels are suppressible by somatostatin and a mixed meal.

Acromegaly↗
PubMed1991

Effect of acute and chronic administration of clonidine on hypothalamic content of growth hormone-releasing hormone and somatostatin in the rat.

Hypothalamic GH-releasing hormone (GHRH) and somatostatin contents were determined in male rats at pre- and mid-pubertal stages following acute (0.15 mg/kg) or chronic (0.1 mg/kg twice daily for 7 days) administration of clonidine. Hypothalamic GHRH content increased markedly during transition from pre- to mid- and late-pubertal stages (2.05 +/- 0.17 vs 3.13 +/- 0.26 and 3.46 +/- 0.20 ng/hypothalamus respectively, means +/- S.E.M.). Hypothalamic GHRH content was markedly decreased 1 h after clonidine administration in mid-pubertal but not in prepubertal rats (3.67 +/- 0.23 vs 2.65 +/- 0.22 ng/hypothalamus). Hypothalamic somatostatin content, on the other hand, decreased in both age groups, although the decrease in the mid-pubertal group was more pronounced (51% and 38% respectively). In addition, the GH responsiveness to clonidine was higher at mid-puberty than at prepuberty. Determination of hypothalamic somatostatin and GHRH content in the chronic experiment 4 h after the last drug administration revealed a marked decrease in GHRH in the mid-pubertal rats and a slight decrease in the prepubertal rats (1.78 +/- 0.32 vs 3.15 +/- 0.31 and 2.01 +/- 0.30 vs 2.35 +/- 0.15 ng/hypothalamus; P less than 0.005 and P less than 0.05 respectively) whereas somatostatin levels were not altered. It is suggested that the clonidine-induced GH secretion is modulated by a chain of events which involves primary stimulation of GHRH release resulting in increased GH secretion which, via a negative-feedback mechanism, triggers an enhancement of somatostatin release which ultimately normalizes the system. This mechanism is age-dependent and reaches full maturity only at the onset of puberty.

Animals↗
PubMed1990

Immunoreactive beta-endorphin, cortisol, and growth hormone plasma levels in obsessive-compulsive disorder.

Basal morning plasma levels of immunoreactive-beta-endorphin (ir-beta-EP), cortisol, and growth hormone (GH) were assessed in 13 obsessive-compulsive disorder (OCD) patients in comparison to 20 healthy controls. All subjects were drug free for at least 1 year. The mean plasma level of ir-beta-EP was significantly lower (36%) in the OCD patients when compared with the control subjects. The decrease in ir-beta-EP was not accompanied by alteration in cortisol and GH plasma levels.

Adolescent↗
PubMed1990

Effect of oral clonidine, insulin-induced hypoglycemia and exercise on plasma GHRH levels in short-stature children.

Human growth hormone release is affected by a variety of pharmacological and physiological stimuli. We have studied the effect of oral clonidine, insulin hypoglycemia, and exercise on plasma hGH and GHRH levels in 31 healthy short-stature children. Thirteen underwent an oral clonidine test (0.15 mg/m2), 12 an iv. insulin test (0.1 U/kg), and 6 performed exercise (running for 10 min in a defined route). GHRH-1-44 was extracted from plasma on silica columns and determined by RIA. Although all three stimuli induced a marked increase in plasma hGH levels, only clonidine induced a significant increase in plasma GHRH levels. Maximal increment in GHRH during clonidine was 6.82 +/- 1.05 pmol/l (mean +/- SEM) as compared with 0.51 +/- 0.28 and 0.53 +/- 0.62 during hypoglycemia and exercise (p less than 0.0005 and p less than 0.005), respectively. An additional 24 subjects received TRH 0.2 mg/kg iv: 8 TRH alone, 8 TRH and insulin, and 8 TRH and clonidine. Only insulin potentiated the TRH-induced TSH response with a peak of 22.0 +/- 3.2 vs 16.0 +/- 0.8 and 15.3 +/- 1.5 mU/l (p less than 0.025) for TRH alone and TRH and clonidine, respectively. It is suggested that clonidine stimulates hGH secretion mainly through an enhancement of GHRH release, whereas stress stimuli such as hypoglycemia and exercise achieve hGH release by a different mechanism, possibly inhibition of somatostatin.

Administration, Oral↗
PubMed1990

Intravenous administration of recombinant IGF-I lowers serum GHRH and TSH.

Recombinant IGF-I was administered as an iv bolus of 75 micrograms/kg to 10 patients with Laron type dwarfism (3 children aged 9, 11 and 12 years and 7 adults aged 30.6 +/- 3.5 years) and to 8 healthy subjects (mean age 19.9 +/- 12.1 years) and determinations of IGF-I, GHRH, hGH, TSH, and glucose were made before and at 2, 5, 15, 30, 60, 90, and 120 min. The following effects were observed: a. an immediate, marked and sustained drop in blood glucose (p less than 0.001), more prolonged in the patients; b. in both groups, a dramatic rise in plasma hGH (p less than 0.01) which peaked at 60-90 min; in the patients this occurred after an initial immediate fall in plasma hGH (p less than 0.01); c. a progressive decrease of plasma GHRH and TSH (p less than 0.05, 0.02) in both patients and healthy controls. An hypothesis is put forward that acute and time-limited release of somatostatin by IGF-I is the main cause of the hormonal changes registered. As the IGF-I bolus also suppressed circulating insulin levels, the hypoglycemia is considered to be a direct effect of IGF-I.

Adult↗
PubMed1988

Plasma cortisol, prolactin, growth hormone, and immunoreactive beta-endorphin response to fenfluramine challenge in depressed patients.

The effect of a single dose (60 mg p.o.) of the serotonin agonistic agent fenfluramine (FNF) on plasma cortisol, prolactin (PRL), growth hormone (GH), and immunoreactive beta-endorphin (ir-beta-EP) levels was assessed in eight major depressed patients and eight controls. The hormones were monitored at basal level (0') and hourly during 5 h following FNF administration. The pharmacological challenge caused an elevation of 80% in PRL secretion in the healthy controls and only 42% in the depressed patients. However, the actual prolactin response (delta max) failed to discriminate depressed patients from controls. A blunted response followed by a decrease (33%) in serum cortisol levels was observed in depressed patients 5 h after drug administration while an increase of 94% was obtained in controls after 3 h. FNF provocation did not affect GH and ir-beta-EP plasma levels. The blunted cortisol responsiveness to FNF administration in depressed patients may reflect functional hypoactivity of central serotonergic system at least during the acute phase of major depression. It is not clear why the cortisol hyporesponsivity in depressed patients is not accompanied by a similar reduced PRL response to FNF challenge.

Adult↗
PubMed1987

Effects of acute and chronic methylphenidate administration on beta-endorphin, growth hormone, prolactin and cortisol in children with attention deficit disorder and hyperactivity.

The effect of 5 mg/p.o. methylphenidate (MPH) challenge on beta-endorphin (beta-EP), growth hormone (GH), prolactin (Prl) and cortisol was investigated in 16 children suffering from attention deficit disorder with hyperactivity (ADDH) before and after 4 weeks MPH treatment. The study population consisted of 13 males and 3 females aged 6-11 years. All patients were drug free for at least 3 months prior to investigation. The severity of ADDH symptomatology and response to MPH chronic treatment was assessed using parent/teacher abbreviated Conners rating scale. Blood samples for beta-EP, cortisol, Prl and GH were drawn before initiation of treatment (basal pre-treatment level), 2 hours after MPH challenge, 4 weeks after MPH treatment (basal post-treatment level) and 2 hours after re-challenge with MPH. Chronic MPH treatment resulted in a decrease in basal Prl levels (5.5 +/- 2.8 vs 3.7 +/- 1.9 ng/ml; p less than 0.05). Pre-treatment challenge stimulates significantly both beta-EP (15.0 +/- 7.5 vs 12.5 +/- 5.3 pmol/l; p less than 0.05) and cortisol secretion (20.6 +/- 6.6 vs 12.6 +/- 5.8 micrograms/dl; p less than 0.05), and suppressed Prl secretion (4.0 +/- 1.5 vs 5.5 +/- 2.8 ng/ml; p less than 0.05). Re-challenge with MPH enhanced beta-EP levels (14.9 +/- 8.6 vs 10.6 +/- 5.0 pmol/l; p less than 0.05) but failed to affect cortisol, Prl and GH secretion. The acute and chronic neuroendocrine effects of MPH administration might be related to its dopaminergic and adrenergic agonistic activity. It might be that the stimulatory effect of single and repeated acute MPH administration on beta-EP release contributes to the beneficial effect of MPH treatment in ADDH children.

Attention Deficit Disorder with Hyperactivity↗
PubMed1987

Cardiorespiratory depression and plasma beta-endorphin levels in low-birth-weight infants during the first day of life.

Twenty-nine premature infants were studied to determine whether neonatal asphyxia, apnea, and low blood pressure in the first day of life are associated with elevated plasma beta-endorphin concentrations. Plasma beta-endorphin levels were determined at 0.5 to 2, 4 to 6, and 18 to 24 hours of life, using radioimmunoassay. Premature infants with moderate or severe asphyxia (n = 19) had higher levels at 0.5 to 2 hours of age (32.1 +/- 6.7 vs 16.4 +/- 7.4 pmol/L) and significantly higher levels at 4 to 6 hours of age (50.4 +/- 10.0 vs 22.9 +/- 9.2 pmol/L) compared with the ten nonasphyxiated premature infants. A significant elevation in levels at age 0.5 to 2 hours (39.4 +/- 9.9 vs 17.7 +/- 4.4 pmol/L) and age 4 to 6 hours (59.3 +/- 13.8 vs 27.1 +/- 17.1 pmol/L) was observed in premature infants with low blood pressure or impaired perfusion (n = 12) who required the administration of volume expanders. No differences were observed in premature infants with and without apnea. It may be speculated that the increased endogenous release of beta-endorphins in response to perinatal asphyxia may play a role in the pathogenesis of shock observed in the first day of life.

Apnea↗
PubMed1987

The effect of acute and repeated electroconvulsive treatment on plasma beta-endorphin, growth hormone, prolactin and cortisol secretion in depressed patients.

The effects of single and repeated electroconvulsive treatment (ECT) on beta-endorphin (beta-EP), cortisol, growth hormone (GH) and prolactin (Prl) plasma levels were investigated in nine depressed patients. Blood samples were monitored a day before ECT, the day of the first and sixth ECT (0, 30, 60 and 90 min after seizures), the day afterwards and 4 weeks after termination of the ECT course. A significant elevation of beta-EP levels was achieved immediately with and 24 h after the first and the sixth ECT. A transient increase in basal beta-EP was observed 1 day following the sixth ECT in comparison with pre-treatment level. Peak and 30 min levels of cortisol were increased compared with baseline by the first ECT. The former (peak) but not the latter (30 min) were increased also at the sixth treatment. GH levels were decreased the day after the first ECT in comparison with the pre-treatment levels and immediately following each ECT in comparison with baseline. A trend toward elevation of Prl was observed immediately after the first and sixth ECT, although the rise did not reach significant levels. ECT administration stimulated beta-EP and cortisol secretion and suppressed human GH release, possibly by activation of endorphinergic and/or serotonergic systems. These mechanisms might be involved in the beneficial effect of ECT in depression.

Adult↗
PubMed1986

Diurnal rhythm of plasma beta endorphin, cortisol and growth hormone in schizophrenics as compared to control subjects.

The diurnal variation of plasma beta endorphin was studied in ten schizophrenics, and in age/sex matched control subjects. In the controls beta endorphin was high in the morning (21.0 +/- 3.5 pmol/l) and decreased towards evening. In the schizophrenic group the beta endorphin fluctuated randomly, ranging within 9-40 pmol/l throughout the day. Plasma cortisol showed a normal diurnal pattern in both groups. The mean plasma cortisol levels in the schizophrenics were significantly higher than in the controls throughout the day. The pattern of plasma human growth hormone (hGH) level was similar in both groups at the time tested. It is hypothesized that the instability of beta endorphin secretion may contribute to the pathogenesis of schizophrenia.

Adult↗
PubMed1985

Effect of clonidine on plasma beta-endorphin, cortisol and growth hormone secretion in opiate-addicted subjects.

The effect of clonidine on plasma beta-endorphin, cortisol and growth hormone was studied in nine opiate-addicted subjects and seven control subjects aged 15 to 37 years. Clonidine, 0.15 mg, was administered orally in the morning, 18 to 24 h after the last administration of opioid drugs. Basal morning beta-endorphin levels were lower in the addicted than in the control subjects (3.76 +/- 0.8 vs. 7.42 +/- 1.2 pmol/l). Following the clonidine, there was an increase to normal values in the addicted subjects, but in the control subjects there was no change. Basal morning levels of cortisol were higher in the addicted subjects than in the controls (21.0 +/- 3.6 micrograms/dl vs. 13.0 +/- 1.2 microgram/dl, mean +/- SE). In control subjects clonidine induced a decrease of 50% in plasma cortisol, whereas in addicted subjects the decrease was not significant. It is hypothesized that in addicted subjects there is impaired activity of endogenous opioid peptides, leading to alteration in beta-endorphin and cortisol secretion.

Adolescent↗
PubMed1985

Comparison of the effect of insulin hypoglycemia and clonidine on secretion of growth hormone, cortisol and beta-endorphin in children and adolescents.

Plasma beta-endorphin, human growth hormone (hGH) and cortisol were measured concomitantly during insulin hypoglycemia (0.1 u/kg i.v.) or clonidine administration (0.075 mg/m2 orally) in children with idiopathic short stature. Whereas hypoglycemia raised plasma beta-endorphin levels, clonidine slightly decreased beta-endorphin in six subjects and had no effect in four. Cortisol levels increased following hypoglycemia and decreased markedly after clonidine. hGH increased to greater than 20 ng/ml in all but one subject. The findings are interpreted as further evidence that the hGH stimulation of clonidine is not stress-mediated.

Adolescent↗