Biomedical subjects

R Volpi

Publications and source records attributed to R Volpi.

At least 73 records · Page 4Linked to original sources

PubMed1995

Dopaminergic and cholinergic control of arginine-vasopressin secretion in type I diabetic men.

Enhanced cholinergic and dopaminergic controls of anterior pituitary function have been described in insulin-dependent diabetes mellitus (IDDM). In order to verify whether similar neurotransmitter alterations also affect the regulation of posterior pituitary hormone secretion, the arginine-vasopressin (AVP) responses to the dopaminergic agonist apomorphine and in a different occasion to physostigmine, an acetylcholinesterase inhibitor, were evaluated in normal (n = 10) and type I diabetics (n = 16). In addition, a control test with normal saline was performed in all subjects. None of the diabetic patients were affected by neuropathy or other diabetic complications. They were divided into two groups according to the duration of their disease (less than 10 years: group 1, n = 8; more than 10 years: group 2, n = 8). Physostigmine (12.5 micrograms kg-1) was infused intravenously over 10 min; apomorphine (60 micrograms kg-1) was injected subcutaneously. Basal AVP concentrations were similar in all groups and remained constant during the control test. In contrast, both drugs induced significant increments in plasma AVP levels in the normal controls and diabetic subjects. However, physostigmine- and apomorphine-induced AVP increments were twofold higher in diabetics than in control subjects. No significant differences were observed between diabetics of groups 1 and 2. No significant correlations between duration of diabetes and peak AVP responses to physostigmine or apomorphine were found within each group or when all diabetic subjects were considered together. These data indicate enhancement of both dopaminergic and cholinergic stimulatory regulations of AVP secretion in patients with uncomplicated IDDM, regardless of the duration of diabetes.

Acetylcholine↗

PubMed1995

Influence of residual C-peptide secretion on the arginine vasopressin response to hypoglycaemia and metoclopramide in insulin-dependent diabetes.

Arginine vasopressin (AVP) hypersecretion in response to metoclopramide or to insulin-induced hypoglycaemia has been described in type I diabetes mellitus. In the present study, we examined whether residual endogenous insulin secretion may play a role in the control of this abnormal AVP secretory pattern. For this purpose, 21 insulin-dependent diabetic men and 10 age- and weight-matched normal men were tested with MCP (20 mg in an i.v. bolus). On a different occasion, subjects were tested with insulin (0.15 IU kg-1). The diabetic patients were subdivided into C-peptide negative patients (CpN, 11 patients without detectable endogenous pancreatic beta cell activity) (group I) and C-peptide positive patients (CpP, 10 patients with residual endogenous insulin secretion) (group II). Experiments started after optimization of the metabolic status of the diabetic men by 3 days of treatment with continuous subcutaneous insulin infusion. The basal concentrations of AVP were similar in all groups. The administration of MCP induced a striking elevation in plasma AVP levels in the normal controls and in the diabetic subjects of groups I and II. However, the AVP rise was significantly higher in group I and group II than in normal controls. Furthermore, group I diabetics showed higher AVP increments than group II. Insulin induced a similar hypoglycaemic nadir in all subjects at 30 min, even though the diabetic subjects of groups I and II had a delayed recovery in blood glucose levels. The hypoglycaemic pattern was similar in group I and II. Hypoglycaemia induced a striking AVP increase in the normal controls.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1994

Inhibitory control of nitric oxide on the arginine-vasopressin and oxytocin response to hypoglycaemia in normal men.

In order to establish whether nitric oxide (NO) participates in the regulation of arginine-vasopressin (AVP) and/or oxytocin (OT) secretion in humans, six normal men were treated with placebo (normal saline) or the NO synthase inhibitor N,G-nitro-L-arginine methyl ester (L-NAME), given at doses (40 micrograms kg-1 injected plus 50 micrograms kg-1 infused i.v.) previously found to be unable to change blood pressure. Experiments were carried out both in basal conditions and during stimulation of posterior pituitary secretion with insulin (0.15 IU kg-1)-induced hypoglycaemia. The administration of saline or L-NAME alone was unable to change basal AVP or OT levels. Insulin-induced hypoglycaemia, however, enhanced plasma AVP and OT levels by two-fold in the absence of L-NAME and by four-fold in the presence of the NO synthase inhibitor (NOS). Blood glucose levels decreased in a similar manner during the insulin tolerance tests, regardless of L-NAME administration. In all experiments, AVP and OT responses to hypoglycaemia followed a similar pattern, with mean peak levels at 45 min. These data suggest that in normal men NO is not involved in regulation of basal AVP and OT secretions, whereas it exerts an inhibitory role in the control of the posterior pituitary hormone responses to hypoglycaemia.

Adult↗

PubMed1994

Naloxone enhances angiotensin II-induced increase in serum luteinizing hormone concentrations in normal women.

The present study was carried out in order to establish whether the stimulatory effect of angiotensin II (ANG II) on serum concentration of LH in women is under control by endogenous opioid peptides. For this purpose, the effect of ANG II (infusion for 60 min of successively increasing doses of 4, 8 and 16 ng/kg/min; each dose for 20 min) on serum LH levels was evaluated during administration of saline or the opioid antagonist naloxone (4 mg in an i.v. bolus followed by 10 mg over 2 h) in 7 normal women in both follicular and luteal phase. In all subjects, tests with saline alone (control test) or naloxone alone were performed. No significant changes in LH levels were observed in any test performed in the follicular phase and in the control test performed in the luteal phase. In contrast, in the luteal phase, both ANG II and naloxone induced significant increments in LH levels (23% increase vs. baseline by ANG II and 54% by naloxone). When naloxone and ANG II were given together stimulated LH increase was greatly enhanced. The mean peak was 154% higher than baseline and was higher than the sum of the individual peaks produced by naloxone and ANG II alone. These findings suggest inhibition by endogenous opioids of the stimulating action of ANG II on LH secretion during the luteal phase.

Adult↗

PubMed1994

Oxytocin response to challenging stimuli in elderly men.

The present study was carried out in order to establish possible alterations in oxytocin (OT) secretion with aging. Therefore, we evaluated the OT responses to insulin (0.15 U/kg)-induced hypoglycemia or to the administration of angiotensin II (i.v. infusion for 60 min of successively increasing doses of 4, 8 and 16 ng/kg min; each dose for 20 min) or apomorphine (60 micrograms/kg s.c.) in male subjects aged 22-80 yr and divided into 3 groups by age (group I (n = 9): 22-38 yr; group II (n = 9): 41-60 yr; group III (n = 9): 63-80 yr). Basal OT concentrations were similar in all groups. The OT response during the insulin tolerance test and the administration of ANG II had similar patterns and magnitudes in all groups. The OT response to apomorphine was similar in the two younger groups, with plasma OT levels increased 118% vs. baseline. In contrast, apomorphine was unable to induce a significant OT rise in the oldest group. During apomorphine test plasma OT concentrations were significantly lower in group III than in groups I and II. For the first time in elderly human subjects, these data show normal responsiveness of the OT secretory system to releasing stimuli such as hypoglycemia and ANG II. These findings indicate that in aged men production of OT and capability of responding to challenging stimuli is unchanged. On the other hand, the reduced OT responsiveness to apomorphine in group III might be an expression of the general dopaminergic dysfunction affecting the aging brain.

Adult↗

PubMed1994

Lack of seasonal variation in abnormal TSH secretion in patients with seasonal affective disorder.

The circadian variations in thyroid-stimulating hormone (TSH) secretion, with particular attention to the nocturnal serum TSH surge and the TSH response to thyrotropin releasing hormone (TRH), were measured in seven patients with seasonal affective disorder (SAD) and in eight normal controls. Both patients with SAD and normal controls were tested in fall/winter, when patients were suffering depressive symptoms, and in spring/summer, when patients were euthymic. The TRH tests were performed in the morning. In all tests, the mean peak TSH response to TRH was significantly lower in the patients with SAD than in the normal controls. No significant differences were observed in either group between spring/summer and fall/winter tests. At both periods, patients with SAD showed normal TSH levels in the morning, but did not experience a nocturnal TSH surge. In this group, morning and night TSH levels were similar. In contrast, normal controls showed significantly higher TSH levels at night than in the morning. Serum-free thyroid hormone levels were in the normal range in all subjects. Morning and night serum cortisol levels and 24-hour urinary cortisol concentrations were similar in all subjects. These data show that the secretion of TSH is impaired in SAD, regardless of the phase of the psychiatric disease. The low TSH response to TRH in the presence of normal serum thyroid hormone levels and the lack of the TSH nocturnal surge suggest that patients with SAD might be affected by mild central hypothyroidism.

Adult↗

PubMed1994

Restoration of ACTH/cortisol and LH responses to naloxone by chronic dopaminergic treatment in Parkinson's disease.

Naloxone is unable to stimulate ACTH/cortisol secretion in patients with de novo Parkinson's disease, suggesting a reduced endogenous opioid control of the hypothalamic-pituitary-adrenal axis in parkinsonian patients. In the present study we examined whether Parkinson's disease also impairs the secretion of LH, which is under the inhibitory control of different opioid peptides than ACTH/cortisol. In addition, we examined whether a chronic dopaminergic therapy for at least one year with levodopa (450 mg/day) plus benserazide (112.5 mg/day) in 3 divided oral doses/day of Madopar modifies the ACTH/cortisol and/or the LH response to naloxone (4 mg as an i.v. bolus plus 10 mg infused in 2 hours). Ten parkinsonian patients (aged 52-62 years) and 8 normal controls (50-60 years) were tested with naloxone and in a different occasion with normal saline. The parkinsonian patients were tested both before and after dopaminergic treatment. Tests started at 09.00 h and lasted 2.5 hours. Basal ACTH/cortisol and LH levels were similar in all groups. During saline tests, ACTH/cortisol levels showed a slight physiological decline in all groups, whereas LH levels remained constant. Naloxone administration significantly increased the plasma levels of ACTH/cortisol and LH in the normal controls, but not in the parkinsonian patients before the dopaminergic treatment. In contrast, dopaminergic therapy restored significant ACTH/cortisol and LH responses to naloxone in parkinsonian patients. In fact, after levodopa plus benserazide, naloxone-induced ACTH, cortisol and LH increments in parkinsonian patients were significantly higher than before therapy and were indistinguishable from those observed in the normal controls. These data suggest that in men Parkinson's-related dopaminergic alterations may underlie the defective endogenous opioid control of ACTH/cortisol and LH secretion.

Adrenocorticotropic Hormone↗

PubMed1994

Endogenous opioid mediation of the inhibitory effect of ethanol on the prolactin response to breast stimulation in normal women.

The effect of ethanol on the prolactin (PRL) response to breast stimulation was tested in normal women. The possible role of endogenous opioids in the control of the PRL response to breast stimulation and ethanol action was also examined. Eleven normal women were tested four times on the 22nd day of four consecutive regular menstrual cycles. All women underwent mechanical breast stimulation (for 10 min) with the concomitant administration of normal saline, naloxone (2 mg in an iv bolus plus 10 mg over 75 min. or 4 mg in an iv bolus plus 20 mg over 75 min.), ethanol (50 ml in 110 ml of whiskey p.o.) or the combination of ethanol and naloxone. Serum PRL levels rose significantly after breast stimulation, with a mean peak response (71.4% higher than baseline at 20 min). The PRL response to breast stimulation was not changed by the treatment with the lower (2 plus 10 mg) or the higher (4 plus 20 mg) dose of naloxone, whereas it was strikingly decreased by ethanol (mean peak was 25% higher than baseline). However, when ethanol was given together with naloxone, the peak rise induced by breast stimulation was only partially inhibited by ethanol (the mean PRL peak was 46.2% higher than baseline). At both doses naloxone produced similar effects. These data demonstrate that ethanol inhibits the PRL response to breast stimulation. Naloxone-sensitive endogenous opioids do not appear to be involved in the control of the PRL rise induced by breast stimulation. In contrast, since naloxone partially reversed the inhibiting effects of ethanol, a partial involvement of opioid peptides in ethanol action is supposed.

Adult↗

PubMed1994

Influence of thyroid status on the paradoxical growth hormone response to thyrotropin-releasing hormone in human obesity.

Thyrotropin-releasing hormone (TRH) tests were performed in 38 age- and weight-matched obese but otherwise healthy men. In all subjects, total thyroxine (T4) and triiodothyronine (T3) concentrations were in the normal range. According to basal and TRH-stimulated serum thyrotropin (TSH) levels, subjects were divided into the following three groups: group I (n = 14), euthyroid subjects; group II (n = 11), euthyroid subjects with normal basal but abnormally elevated TSH responses to TRH; group III (n = 13), subjects with elevated basal and TRH-induced TSH levels (subclinical hypothyroidism). Basal TSH levels were 1.8 +/- 0.4 mU/L in group I, 1.7 +/- 0.3 in group II, and 6.0 +/- 0.7 in group III. In both groups II and III, TRH-induced TSH increments were above the normal range (maximal increment > 14 mU/L) and were significantly higher than in group I. The definition of euthyroidism for groups I and II and of subclinical hypothyroidism for group III according to the basal levels of TSH was confirmed by clinical (Billewicz index), hormonal (serum free-T4 levels), and metabolic (serum apoprotein [apo] AI levels) parameters. Basal concentrations of growth hormone (GH) were similar in all groups. When GH levels after TRH stimulation were measured, significant increments (peak minus baseline > 5 micrograms/L) were observed in nine of 13 hypothyroid obese men. The overall mean peak GH increase in group III was 4.5 times higher than baseline and was observed at 45 minutes. None of the euthyroid obese subjects of groups I and II showed any significant change in GH levels in response to TRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Growth Hormone↗

PubMed1994

Different effects of delta-sleep-inducing peptide on arginine-vasopressin and ACTH secretion in normal men.

UNLABELLED: Delta-sleep-inducing peptide (DSIP) is a well-known inhibitor of pituitary ACTH secretion. In order to evaluate the possible influence of DSIP on basal arginine-vasopressin (AVP) secretion and/or on the AVP-response to osmotic and pressure/volumetric stimuli, DSIP (25 nmol/kg) was infused in 10 min to 8 normal men (23-34 years old) just before a 2-hour infusion of normal saline (NaCl 0.9%; DSIP test) or hypertonic saline (0.51 M NaCl; osmotic test) or before an orthostatic test (standing upright and maintaining an orthostatic position for 20 min). In different occasions, a 10-min infusion of normal saline (placebo) was given instead of DSIP. In an additional 7 subjects, DSIP or placebo was given 60 min before hypertonic saline or the orthostatic test. The results obtained after the administration of DSIP at time 0 and at -60 min were similar. RESULTS: The administration of DSIP or normal saline alone did not change the concentrations of circulating AVP. A slight physiological decline in ACTH levels was observed during saline infusion, whereas a significant decrease in ACTH levels was induced by DSIP administration. Osmotic stimulation of AVP secretion by hypertonic NaCl induced a significant increase in plasma AVP concentrations which was not modified by DSIP administration. The ACTH secretory patterns during hypertonic NaCl and hypertonic NaCl plus DSIP were similar to those observed during normal saline and normal saline plus DSIP, respectively. The orthostatic test provided similar plasma AVP increments, regardless of the previous treatment with DSIP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1994

Opioid modulation of the gamma-aminobutyric acid-controlled inhibition of exercise-stimulated growth hormone and prolactin secretion in normal men.

The possible involvement of endogenous opioids in the gamma-aminobutyric acid-controlled (GABAergic) inhibition of growth hormone (GH) and prolactin (PRL) during physical exercise was evaluated in normal men. After fasting overnight, seven subjects were tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. The workload was gradually increased at 3-min intervals until exhaustion and lasted about 15 min in all subjects. Tests were carried out under administration of placebo, the opioid antagonist naloxone (10 mg as an iv bolus injection), the GABAergic agonist sodium valproate (600 mg in three divided doses orally) or naloxone plus sodium valproate. During exercise, plasma GH and PRL levels rose 5.5- and 1.9-fold, respectively. The administration of naloxone did not modify, whereas sodium valproate significantly reduced the plasma GH and PRL rise during exercise. In the presence of sodium valproate, GH and PRL levels rose 3- and 1.5-fold, respectively, in response to exercise. When naloxone was given together with sodium valproate, both GH and PRL responses to exercise were abolished completely. These data suggest the involvement of a GABAergic mechanism in the regulation of GH and PRL responses to physical exercise in men. Furthermore, the data argue against a role of naloxone-sensitive endogenous opioids in the control of these hormonal responses to exercise, whereas they suggest a modulation by opioids of the GABAergic inhibitory action.

Adult↗

PubMed1993

Role of GABA and opioids in the regulation of the vasopressin response to physical exercise in normal men.

The present study was undertaken in order to establish the possible involvement of GABAergic and/or opioid pathways in the mechanism underlying the arginine-vasopressin (AVP) response to physical exercise. After fasting overnight, seven subjects were tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. The workload was gradually increased at 3 min intervals until exhaustion and lasted about 15 min in all subjects. Tests were carried out under administration of placebo, the opioid antagonist naloxone (10 mg as an i.v. bolus injection), the GABAergic agonist sodium valproate (600 mg in three divided doses orally) or naloxone plus sodium valproate. Plasma AVP levels rose 4-fold during exercise. The administration of naloxone did not modify, whereas sodium valproate completely abolished the plasma AVP rise during exercise. When naloxone was given together with sodium valproate, AVP rose 3-fold in response to exercise. These data suggest the involvement of a GABAergic mechanism in regulation of the AVP response to physical exercise in men. Furthermore, the data argue against a role of naloxone sensitive endogenous opioids in the control of AVP during exercise, whereas they suggest a partial opioid mediation of the GABAergic inhibitory action.

Adult↗

PubMed1993

Lack of ACTH/cortisol and GH responses to intravenously-infused substance P in Parkinson's disease.

In order to test possible changes in the stimulating effect of intravenously-infused substance P (SP) on ACTH/cortisol and GH secretion in Parkinson's disease, 10 male parkinsonian patients and 10 age-matched normal controls were infused intravenously for 60 min with SP (1.0 or 1.5 pmol/kg-1/min-1 SP) or normal saline. The circulating levels of ACTH, cortisol and GH were measured during and for 20 min after SP or saline infusion. No untoward side effects or changes in blood pressure were observed during SP infusion in any subjects. In basal conditions and during saline infusion, plasma ACTH and cortisol levels were similar in normal and parkinsonian patients. During SP infusions, ACTH/cortisol concentrations in normal controls rose significantly vs baseline and saline test in a dose-dependent fashion. In contrast, at both SP infused amounts, parkinsonian patients showed ACTH/cortisol levels similar to those observed in the saline test. All subjects showed similar basal concentrations of GH. GH levels rose significantly in the normal controls when the higher dose of SP was infused, but they were not modified by the infusion of the lower dose of SP or saline. At both tested amounts of SP and during saline infusion, GH levels remained unchanged in the parkinsonian subjects. In agreement with previous observations in the literature showing SP abnormalities in the parkinsonian brain, these data fail to show significant effects of plasma SP on the ACTH/cortisol and GH secretory systems in Parkinson's disease.

Adrenocorticotropic Hormone↗

PubMed1993

Gamma-aminobutyric acid mediation of the inhibitory effect of endogenous opioids on the arginine vasopressin and oxytocin responses to nicotine from cigarette smoking.

Previous studies have demonstrated that naloxone exerts positive effects on the responsiveness of arginine vasopressin (AVP) and oxytocin (OT) to nicotine, suggesting inhibitory actions of endogenous opioids. The present study was designed to determine whether a gamma-aminobutyric acid (GABA)ergic pathway is involved in the regulation of naloxone-sensitive endogenous opioid action. AVP and OT secretory patterns after (two nonfilter) cigarette smoking were examined in seven normal male subjects with (experimental test) and without (control test) concomitant treatment with naloxone (4 mg in an intravenous bolus plus 6 mg infused over 2 hours), the GABAergic agent sodium valproate (600 mg in three divided doses orally), or the combination of naloxone and sodium valproate. Cigarette smoking increased by 2.4-fold (peak v baseline) the plasma concentrations of AVP without modifying OT levels. In the presence of naloxone, plasma AVP and OT levels in response to nicotine were significantly higher than those in the control test. In the naloxone plus nicotine test, AVP levels increased 4.2-fold (peak v baseline) and OT concentrations increased 1.6-fold (peak v baseline). Pretreatment with sodium valproate changed neither AVP nor OT secretory patterns during the cigarette-smoking test. In contrast, sodium valproate abolished the facilitating effect of naloxone on both AVP and OT responses to nicotine. In the sodium valproate plus naloxone plus nicotine test, plasma AVP and OT levels were not significantly higher than those obtained during the nicotine test. These data indicate a GABAergic mediation of the inhibitory modulation by endogenous opioids of the AVP and OT responses to nicotine.

Adult↗

PubMed1993

Abnormal serotonergic control of prolactin and cortisol secretion in patients with seasonal affective disorder.

The effects of the serotonergic agent d,l-fenfluramine (60 mg PO) or a placebo on serum prolactin (PRL) and cortisol levels were evaluated in seven patients (five men and two women) with seasonal affective disorders (SAD) and in eight normal controls (eight men and two women). Both groups were tested in fall/winter when patients with SAD suffered depressive symptoms and in spring/summer, when patients were euthymic. Spring/summer and fall/winter tests gave similar results. PRL and cortisol patterns were similar in all subjects after placebo, whereas both hormonal responses to d,l-fenfluramine were significantly lower in patients with SAD than in normal controls. Correlation studies between the two hormonal responses revealed that on both periods the amplitudes of PRL and cortisol increments were significantly and positively correlated in patients with SAD. These data show diminished serotonergic responsiveness in SAD regardless of the actual depressive status of the patients. They are consistent with a decrease of central serotonergic activity in SAD.

Adult↗

PubMed1993

Reduction in the arginine vasopressin responses to metoclopramide and insulin-induced hypoglycemia in normal weight bulimic women.

A low plasma arginine vasopressin (AVP) responsiveness to hypertonic saline infusion has been described in bulimic women. At present, it is unknown whether this phenomenon is peculiar for the osmotic regulation of AVP secretion or whether it represents an aspect of a more general disorder of AVP secretion in bulimia nervosa. In order to answer these questions, in the present study the AVP responses to metoclopramide (MCP) (20 mg in an i.v. bolus) and insulin (0.15 IU/kg)-induced hypoglycemia were tested in normal weight bulimic women and in weight- and age-matched normal women. Basal AVP concentrations were similar in normal and bulimic women. In the normal controls, plasma AVP levels rose 2.6 times after MCP and 2.2 times in response to hypoglycemia. Both AVP increments were significantly lower in bulimic patients. In this group, plasma AVP levels rose 2 times after MCP and 1.8 times in response to hypoglycemia. When data of the MCP and insulin tolerance test were combined, regression analyses showed a significant positive correlation between AVP peak responses to MCP and hypoglycemia in the bulimic group. These data show an impaired AVP response to different releasing stimuli in bulimia, suggesting that a more general disorder than a simple change in the sensitivity to osmotic stimulation affects the AVP secretory system in bulimic patients. It is likely that bulimic subjects are affected by a neuroendocrine alteration in the control of AVP secretion, whose mechanisms are still unknown.

Adult↗

PubMed1993

Intravenously infused substance P is unable to change basal and TRH-stimulated PRL secretion in normal men.

In order to test the possible effects of an intravenous administration of substance P (SP) on basal and TRH-stimulated PRL release, SP was infused alone (0.5 or 1.5 pmol/kg-1/min-1 for 60 min) or after TRH (20 or 400 micrograms in an i.v. bolus) in 21 normal male subjects. In addition, plasma cortisol levels during SP infusion were measured. In agreement with previous findings, a significant increase in plasma cortisol levels was observed when the higher (1.5 pmol/kg-1/min-1) but not the lower (0.5 pmol/kg-1/min-1) amount of SP was given. In contrast, basal and TRH (20 or 400 micrograms)-induced PRL release were not modified by SP at any tested amount. These data suggest that, in normal men, plasma SP is not involved in the control of PRL release at the anterior pituitary level.

Adult↗

PubMed1992

Hyperthermia in sauna is unable to increase the plasma levels of ACTH/cortisol, beta-endorphin and prolactin in cocaine addicts.

In order to establish possible different reactions between normal subjects and cocaine addicts to short term exposure to heat, thermal, cardiovascular and pituitary hormonal responses to hyperthermia in sauna were measured in 8 male cocaine addicts (studied after 14 days of abstinence) and in 8 age and weight matched normal men. Subjects sat for 30 min in a sauna room, where the temperature was 90 C and the relative humidity 10%. Physiological and hormonal parameters were measured just before and after sauna and after 30 min of rest at normal (21 C) room temperature. Significant and comparable increments in systolic and diastolic blood pressure, pulse rate and sublingual temperature were observed in the two groups at the end of sauna. All these parameters decreased to normal values after 30 min of rest at normal room temperature. Before sauna, ACTH, cortisol and beta-endorphin levels were similar in the two groups, whereas plasma prolactin concentrations were significantly higher in cocaine addicts. All examined hormones rose significantly in the normal controls at the end of sauna. All hormones, except cortisol, returned to the basal levels after 30 min at normal room temperature. In contrast, no significant hormonal responses to hyperthermia were observed at any time point in cocaine addicts. These data do not provide evidence of alterations in the cardiovascular and thermal adaptive responses to hyperthermia in cocaine abusers. On the other hand, the results show an impairment of the ACTH/cortisol, beta-endorphin and prolactin responses to hyperthermia in cocaine addicts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗