Biomedical subjects

V Coiro

Publications and source records attributed to V Coiro.

At least 91 records · Page 5Linked to original sources

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

Cerebral atrophy and plasma cortisol levels in alcoholics after short or a long period of abstinence.

Basal cortisol levels were significantly lower in 4 week abstinent alcoholics (n = 11; group A) than in normal controls (n = 9; group C), whereas no significant difference was found between alcoholics abstinent greater than 1 year (n = 9; group B) and controls. In all groups, dexamethasone induced a similar decrease in circulating cortisol concentrations. Computed tomographic examinations showed a significantly higher ventricular-brain ratio VBR) and wider 3rd ventricle width in group A than in group B; no significant differences were observed between groups B and C. In contrast, the number of cerebral sulci was similar in all groups. A negative relationship was found between neuroradiological findings and basal cortisol values in group A, but not in groups B and C. The neuropsychological tests showed worse scores in group A than in the other groups. These findings show subcortical damages and reduced cortisol levels in alcoholics after 4 weeks of abstinence. These alterations appear to be at least in part reversible after a long period of abstinence.

Adult↗

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

Hyperthermia and endorphins.

This paper discusses the role of endogenous opioids in response to hyperthermia and the alterations observed in drug or alcohol addicts. Endorphins, rather than enkephalins are involved in adaptation to heat in the central nervous system. The pituitary secretion of beta endorphin together with ACTH in response to thermal stress provided the opportunity to measure the opioid reactivity to hyperthermia in health and toxicomania, as an index of opioid function, in adaptation to heat. The review of the data in the literature shows absent responses of beta endorphin and its related hormone ACTH to the thermal stress of sauna in heroin, cocaine or alcohol addicts. A common explanation for this phenomenon is that the long-term stimulation of hypothalamic opioid neurotransmission that is produced directly or indirectly by heroin, alcohol or cocaine, disrupts the opioid response to thermal stress, and thus the adaptation to heat.

Adrenocorticotropic Hormone↗

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

Effects of intravenous infusion of substance P on arginine vasopressin and oxytocin secretion in normal men.

In order to establish possible stimulatory effects of increasing plasma concentrations of substance P (SP) on the arginine vasopressin (AVP) and/or oxytocin (OT) secretion, successively increasing doses of SP(0.5, 1 and 1.5 pmol/kg-1/min-1; each dose for 20 min) were infused in 7 normal men. Plasma AVP and OT levels were measured before infusion and every 20 min, just before increasing the infusion dose of SP. During tests, SP infusion did not produce untoward side effects or changes in blood osmolality and/or pressure. Plasma OT levels did not change during SP infusion. Plasma AVP concentrations were not modified by the infusion of the lowest dose of SP, whereas they were significantly increased in a dose response fashion when higher amounts of SP were given. These findings demonstrate for the first time in humans that the systemic administration of SP exerts stimulatory effects on AVP, but not on OT secretion.

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↗

PubMed1992

Inhibitory effect of dexamethasone on the oxytocin response to insulin-induced hypoglycemia in normal men.

Glucocorticoids are known to reduce both ACTH and arginine vasopressin responses to insulin-induced hypoglycemia in normal men. The present study was undertaken in order to establish whether glucocorticoids are capable of modifying the oxytocin (OT) response to hypoglycemia. For this purpose, 8 normal men (28-33 yr) were tested with insulin (0.15 IU/kg in an iv bolus) [insulin tolerance test (ITT)] with and without pretreatment with dexamethasone (2 or 4 mg in an iv bolus 10 min before insulin). Eight different subjects (29-35 yr) were tested with dexamethasone alone. The administration of dexamethasone (2 or 4 mg) alone changed neither ACTH nor OT concentrations in the plasma during the next hour. Insulin produced similar hypoglycemic responses, regardless of dexamethasone treatment. ACTH levels rose significantly in response to insulin-induced hypoglycemia, with a mean peak response at 45 min (p less than 0.01 vs baseline). Two and four mg dexamethasone produced similar significant reductions of the ACTH response to hypoglycemia (p less than 0.02 at 45 min, p less than 0.05 at 30 and 60 min vs ITT). In the ITT, OT levels rose significantly in response to hypoglycemia, with a mean peak response at 45 min (p less than 0.01 vs basal value). The pretreatment with 2 or 4 mg dexamethasone reduced in a similar manner the hypoglycemia-induced OT rise (p less than 0.05 at 30 and 45 min vs ITT). These findings show a partial inhibition by dexamethasone of the OT response to hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1992

Failure of the gamma-aminobutyric acid (GABA) derivative, baclofen, to stimulate growth hormone secretion in heroin addicts.

In order to establish possible alterations in the gamma aminobutyric acid (GABA)ergic control of growth hormone (GH) secretion in heroin addicts, ten patients (age, 25.8 +/- 1.07 yr (mean +/- SE); duration of heroin addiction, range 3-8 yr; weight, 67.3 +/- 0.87 kg body weight), and ten age (29.1 +/- 0.84 yr)- and weight (69.7 +/- 0.87 kg)-matched normal controls were tested with the GABAergic B-receptor agonist baclofen (10 mg p.o. at 09.00 h) (experimental test) or a placebo (control test). Blood samples for GH assay were taken every 15 min for the next 150 min. Normal controls underwent one control and one experimental test. Heroin addicts were submitted to both baclofen and placebo test twice, once around the time of their admission to a recovery community for drug abusers, when they were still assuming heroin, and again after two months of permanence in the community. From the time of their admission to the community, the patients were forbidden to use heroin. For two weeks after admission they were treated with clonidine and acetylsalicilic acid to attenuate withdrawal symptoms. Thereafter, the patients underwent a period of wash-out of pharmacological treatments for at least 6 weeks before being retested. Basal GH levels were similar in normal controls and heroin addicts in all tests and remained unmodified during control tests in all subjects. The administration of baclofen increased four times the serum GH levels within 120 minutes in the normal controls, whereas it did not modify serum GH concentrations in heroin addicts either during the period of drug abuse or after two months of abstinence. These data show that the control of GH secretion mediated by GABAergic B-receptors is impaired in heroin addicts. It is hypothesized that this neuroendocrine alteration might represent a trait marker of heroin addiction, or more likely, that it was a consequence of a long addiction to heroin persisting after two months of abstinence.

Adult↗

PubMed1992

Luteinizing hormone response to an intravenous infusion of substance P in normal men.

The effect of synthetic substance P (SP), infused intravenously in doses of 0.5, 1.0, or 1.5 pmol/kg-1/min-1 for 60 minutes, on gonadotropin secretion was evaluated in seven healthy men. SP tests and a control test with normal saline were randomly performed at weekly intervals. During the tests, SP infusion did not produce untoward side effects or changes in blood pressure. Plasma testosterone concentrations were normal in all subjects and remained unmodified during all tests, regardless of the infused dose of SP. Plasma luteinizing hormone (LH) levels were not modified when either normal saline or the lowest dose of SP were infused, whereas they were significantly increased in a dose-dependent fashion when larger amounts of SP were administered. In contrast, plasma follicle-stimulating hormone (FSH) concentrations did not change significantly during any test. These data demonstrate for the first time in normal men that the systemic infusion of SP stimulates LH release, without modifications of FSH secretion.

Adult↗

PubMed1992

ACTH and beta-endorphin responses to physical exercise in adolescent women tested for anxiety and frustration.

Thirty healthy adolescent women (age: 14 years), high school students without clinical signs of psychiatric or major affective disorders, received psychological and endocrinological examinations. Two psychological tests were used: the Anxiety Score Test for Adolescents and the Pictures Frustration Test for Adolescents of Rosenzweig. On the basis of the results of these tests, subjects were divided into two groups: A (n = 21), normal subjects; B (n = 9), subjects with evidence of anxiety (n = 1), frustration (n = 1), or both (n = 7). Plasma levels of adrenocorticotropic hormone (ACTH) and beta-endorphin were measured under basal conditions and after physical exercise (Step Test) in all subjects. Hormonal responses in groups A and B were compared. Basal concentrations of ACTH and cortisol were similar in the two groups, whereas basal beta-endorphin levels were significantly higher in group B than in group A. Exercise induced a slight but significant increase in plasma concentrations of both ACTH (32% increase) and beta-endorphin (60% increase) in group A. A striking increase in plasma ACTH (100% increment) and a slight increase of beta-endorphin (60% increment) levels were observed in group B after exercise. Absolute levels of ACTH and beta-endorphin after physical exercise were significantly higher in group B than in group A. These findings indicate increased levels of adrenocorticotropic and opioid activity in adolescent women with high scores on psychological measures of anxiety and frustration.

Adolescent↗