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Biomedical subjects

V Coiro

Publications and source records attributed to V Coiro.

At least 145 records · Page 8Linked to original sources
PubMed1989

Abnormal thyroid stimulating hormone, prolactin, and growth hormone responses to thyrotropin releasing hormone in abstinent alcoholic men with cerebral atrophy.

The thyroid stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH) responses to thyrotropin releasing hormone (TRH), the Wechsler Adult Intelligence Scale (WAIS) for cognitive impairment, and computed tomographic scans were evaluated in 15 nondepressed alcoholic men after 4 weeks of abstinence and in 10 normal controls. Both cognitive impairment and cerebral atrophy were found in 13 of the alcoholics. Eight alcoholics (seven with cerebral atrophy) had blunted TSH and PRL responses to TRH and a TRH-induced paradoxical increase of GH. This study demonstrates that besides affecting the TSH response to TRH, alcoholism often induces alterations of the PRL and GH secretory patterns in response to TRH. The severe brain damage caused by long-term alcoholism might be involved in the pathogenesis of these neuroendocrine alterations.

Adult↗
PubMed1989

Dopaminergic, but not cholinergic, involvement in regulation of hypoglycemia-induced oxytocin release in man.

The plasma oxytocin response to insulin-induced hypoglycemia was evaluated in 20 normal male subjects in the basal state (insulin tolerance test (ITT) alone) and after pretreatment with the muscarinic antagonist pirenzepine (40 mg IV 10 min before the ITT in six subjects), the nicotinic antagonist trimethaphan (0.3 mg/min IV for 30 min before the ITT in six subjects), and the dopaminergic receptor agonist bromocriptine (2.5 mg PO 1 hr before the ITT in eight subjects). The drugs did not modify arterial blood pressure nor produce side effects capable of altering oxytocin secretion. Neither pirenzepine nor trimethaphan administration changed the oxytocin response to hypoglycemia, whereas bromocriptine significantly reduced the oxytocin increase during the ITT. These data suggest the involvement of dopaminergic, but not of cholinergic, muscarinic or nicotinic, receptors in the oxytocin response to hypoglycemia.

Adult↗
PubMed1989

Effects of ovariectomy on blood and plasma viscosity, fibrinogen and whole blood filterability.

Blood and plasma viscosity, fibrinogen concentrations and whole blood filterability (VB) were evaluated before surgery and 7 and 30 days postoperatively in 2 groups of subjects, one of which comprised 10 hysterectomized women and the other 14 women who had undergone both hysterectomy and ovariectomy. Oestrogens and various metabolic haematological parameters were measured and correlated with the haemorrheological data. By day 7 after surgery fibrinogen concentrations and plasma viscosity had increased, while VB had decreased. Plasma viscosity and fibrinogen levels correlated negatively with VB in the non-ovariectomized women. Three weeks later almost complete normalization of all parameters was observed in all of the subjects, except for the persistence of low oestrogen concentrations and a further decrease in VB values in the ovariectomized patients, these parameters showing a positive correlation. This study demonstrates that haemorrheological alterations occur after hysterectomy (with or without ovariectomy) in the early post-operative period. The striking decrease in VB values and its correlation with the oestrogen concentrations observed 1 mth after ovariectomy suggest that the fall in oestrogen levels might be responsible for the decrease in whole blood filterability.

Adult↗
PubMed1989

Effects of the GABAergic agent sodium valproate on the arginine vasopressin responses to hypertonic stimulation and upright posture in man.

In order to evaluate the possible influence of GABAergic neurotransmission on the arginine vasopressin (AVP) response to osmotic and pressure volumetric stimuli, the GABAergic drug sodium valproate was administered by mouth (200 or 400 mg 16 h, 8 h and just before tests) to eight normal men before osmotic (i.v. infusion of 0.51 , NaCl for 2 h) and orthostatic (standing upright and maintaining an orthostatic position for 20 min) tests. In both experimental conditions, the AVP rise was significantly lower in the presence than in absence of sodium valproate. The maximum AVP responses in the control orthostatic and osmotic tests were respectively 2.3 and 2.5 times higher than basal levels. When 600 mg sodium valproate was given, the maximum AVP rise in response to hypovolaemic and osmotic stimuli were respectively 1.75 and 2.1 times higher than basal value. Similar results were obtained giving 1.2 g sodium valproate. These results suggest that in man a GABAergic pathway is involved in the AVP responses to hypovolaemic and hyperosmotic stimuli.

Adult↗
PubMed1989

Muscarinic cholinergic, but not serotoninergic mediation of arginine vasopressin response to metoclopramide in man.

The possibility that metoclopramide (MCP) stimulates arginine vasopressin (AVP) secretion in man through a serotoninergic and/or a cholinergic muscarinic pathway was studied. Twenty normal male subjects were tested with MCP (10 mg in an i.v. bolus) alone or in the presence of the 5HT1 serotoninergic antagonist metergoline (10 mg/day p.o. in five divided doses for 4 days), the 5HT2 receptor blocker ketanserin (10 mg i.v. 5 min before MCP) (n = 10), the M1 and M2 muscarinic antagonist atropine (1.2 mg i.v. just before MCP administration) or the M1 muscarinic receptor blocker pirenzepine (40 mg i.v. 10 min before MCP) (n = 10). AVP doubled in response to MCP. the MCP-induced AVP rise did not change after metergoline, ketanserin or pirenzepine administration, whereas it was abolished by atropine. Additional experiments were performed in order to evaluate the effect of 1.2 mg atropine, given alone, on circulating AVP levels and whether the effect of atropine on the AVP response to MCP depends on the amount of the muscarinic antagonist (dose-response study). For these purposes, atropine was given alone to the same subjects previously tested with MCP plus atropine; furthermore, eight additional male subjects were tested with MCP plus atropine given in doses ranging from 0.8 to 1.4 mg. The results of these additional studies failed to show an effect of atropine alone on AVP secretion and demonstrated a dose-related inhibition of MCP-induced AVP rise by increasing atropine administration from 0.8 mg to 1.2 mg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Different effects of aging on the opioid mechanisms controlling gonadotropin and cortisol secretion in man.

The present study was undertaken in order to assess the influence of aging on the endogenous opioid control of gonadotropin and adrenocorticotropin/cortisol secretion in man. For this purpose, the capability of the opioid antagonist naloxone to increase circulating levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and cortisol was tested in male subjects of different ages. Thirty normal men were randomly chosen and divided into 3 groups by age: group I = 22-40 years (n = 10); group II = 41-59 years (n = 10); group III = 62-80 years (n = 10). Since the men of group III showed higher basal serum gonadotropin concentrations than the subjects of group I and group II, we selected from a large population a fourth group of elderly men with normal basal LH and FSH levels: group IV = 61-82 years (n = 7). All subjects were tested for 120 min during the intravenous administration of naloxone (4 mg given in an intravenous bolus at time 0, plus 10 mg infused for 2 h). Control tests with normal saline instead of naloxone were performed in all groups. All subjects had similar blood testosterone and cortisol levels, whereas LH and FSH concentrations were significantly higher in group III than in groups I, II and IV. Naloxone increased plasma cortisol concentrations by 50% in all groups. The cortisol secretory response followed a similar pattern regardless of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1989

Simultaneous inhibition by pirenzepine of the GH responses to GnRH and TRH in insulin-dependent diabetics and in patients with major depression.

The present study was undertaken in order to establish whether muscarinic cholinergic receptors are involved in the anomalous GH response to GnRH in men with insulin-dependent diabetes mellitus and in male patients with major depression. For this purpose, 16 male diabetics, 18 depressed men and 9 normal controls were tested with GnRH (25 micrograms iv) with and without previous treatment with the muscarinic cholinergic receptor blocker pirenzepine (40 mg iv 10 min before GnRH). Additional experiments with TRH (200 micrograms iv 10 min after pirenzepine) were performed in the same subjects and used for comparison between responders to TRH and GnRH. The administration of GnRH stimulated GH release in 12 out of the 16 diabetics and in 8 out of the 18 depressed patients, but not in the normal controls. Control and diabetic non-responders to GnRH did not respond to TRH. In contrast, all diabetic responders to GnRH, except 2, showed paradoxical GH responses to TRH. All depressed responders to GnRH and 3 of the non-responders, were responsive to TRH. The pattern and magnitude of the secretory responses to TRH and GnRH were similar in depressed and diabetic patients. When the effects of GnRH and TRH were restudied in the presence of pirenzepine, neither GnRH nor TRH enhanced the serum concentrations of GH in any patient. These data indicate that a muscarinic cholinergic mechanism is involved in the anomalous responses of GH to GnRH and TRH in diabetic men and in male patients affected by major depression.

Acetylcholine↗
PubMed1989

Arginine vasopressin secretion in non-obese women with polycystic ovary syndrome.

Arginine vasopressin responses to osmotic (0.1 ml.kg-1.min-1 NaCl), orthostatic (standing upright and maintenance of orthostatic position for 20 min), and hypoglycemic (0.15 IU/kg insulin) stimuli were evaluated in women with polycystic ovaries and in normal subjects. Blood dehydroepiandrosterone, dehydroepiandrosterone sulphate, androstenedione, testosterone, cortisol, and endogenous insulin levels were significantly higher in women with polycystic ovaries than in controls, whereas estrone, estradiol-17 beta, progesterone and 17OH-progesterone concentrations were normal in all subjects. Arginine vasopressin basal levels (mean +/- SEM of 3 test days; women with polycystic ovaries: 2.8 +/- 0.2 pmol/l; controls: 2.7 +/- 0.2 pmol/l) and secretory responses to orthostatic (mean peaks 100% higher than baseline values) and to hypertonic (130% increments) stimuli were similar in the two groups. Arginine vasopressin responses to hypoglycemia were lower in women with polycystic ovaries (50% increment) than in controls (150% increment), although comparable blood glucose decrements and GH or cortisol increments were found in the two groups. Arginine vasopressin peak responses to hypoglycemia were negatively correlated to testosterone, androstenedione, and endogenous insulin levels, but did not correlate with basal and hypoglycemia-induced peak cortisol concentrations or with circulating levels of other steroids. These data indicate a hypothalamic posterior pituitary disorder affecting arginine vasopressin response to insulin-induced hypoglycemia in women with polycystic ovaries syndrome associated with elevated blood androgen and insulin concentrations.

Adult↗
PubMed1988

Oxytocin response to insulin-induced hypoglycemia in obese subjects before and after weight loss.

The response of plasma oxytocin to an iv bolus injection of crystalline insulin (0.15 U/kg) was evaluated in 14 normal weight [mean body mass index (BMI) = 23] and in 9 obese (mean BMI = 42) men. Similar blood glucose decrements after insulin injection were observed in the two groups. Obese and normal weight subjects presented similar basal oxytocin levels. In both groups, oxytocin rose significantly during the insulin tolerance test (ITT); however, the peak oxytocin response in the obese men was significantly lower than in the normal weight subjects. Obese men were restudied after substantial weight loss. Basal oxytocin levels and glucose response to insulin did not change after weight reduction. The oxytocin response to the ITT was significantly higher than before slimming and did not differ from that observed in the normal weight subjects. A significant negative correlation between BMI values and oxytocin peak levels during ITT was observed in the lean controls and obese subjects (r = 0.516, p less than 0.02). These results demonstrate that in obese subjects the oxytocin secretory response during an insulin tolerance test is reduced, suggesting the existence of a hypothalamic-pituitary disorder in obesity.

Adult↗
PubMed1988

Oxytocin reduces exercise-induced ACTH and cortisol rise in man.

The effect of oxytocin on the ACTH, cortisol, GH and PRL response to physical exercise was investigated in 6 normal men. In addition, the possible involvement of endogenous opioids in the mediation of oxytocin action was evaluated. After fasting overnight, each subject was 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 20 min in all subjects. Tests were carried out under administration of oxytocin (2000 mIU as an iv bolus injection plus 32 mIU/min per 30 min) or naloxone (10 mg as an iv bolus injection) alone; furthermore, the effect of oxytocin together with naloxone (10 mg as an iv bolus injection) was evaluated. In the remaining test, normal saline was given instead of drugs. Plasma ACTH, cortisol, PRL and GH concentrations were significantly increased by physical exercise. Administration of oxytocin, naloxone or their combination was without effect on the PRL and GH rise elicited by exercise. In contrast, the exercise-induced ACTH and cortisol response was significantly raised by naloxone and reduced by oxytocin. When oxytocin was preceded by administration of naloxone, the ACTH and cortisol response to exercise was not reduced by oxytocin. These data show that oxytocin is capable of inhibiting the rise in ACTH and cortisol, but not in GH and PRL induced by physical exercise. Since naloxone abolished the inhibitory effect of oxytocin, oxytocin action on ACTH and cortisol secretion might be supposed to be mediated by an opioid pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1988

Effect of bromocriptine on neurophysin secretion in pregnant women in labour.

In order to determine whether dopamine plays a role in the control of neuropituitary function in pregnant women during labour, blood levels of nicotine (NSN)- and estrogen (ESN)-stimulated neurophysins were measured in 119 women treated orally with placebo (n = 59, control group) or 5 mg bromocriptine, a potent dopaminergic receptor agonist (n = 60, experimental group). Serum samples were taken before drug ingestion (basal sample) and at delivery. The serum basal concentrations of NSN and ESN were similar in both groups of pregnant women in labour. At delivery, serum ESN levels were similar in all women regardless of the treatment, whereas NSN concentrations were significantly lower in the bromocriptine-treated women than in those who were given placebo. In additional experiments the effect of 5 mg bromocriptine on the serum concentrations of NSN and ESN was tested for 6 hours after drug ingestion in 10 healthy, non-pregnant women and in 8 women in the 3rd trimester of pregnancy. Bromocriptine did not modify the circulating levels of NSN and ESN in either of these 2 groups of women. Since NSN and ESN are thought to be associated with vasopressin and oxytocin, respectively, these results indicate that in non-pregnant women and in pregnant women during late pregnancy dopaminergic stimulation with a dopaminergic receptor agonist does not inhibit the release of either vasopressin or oxytocin during rest. In contrast, dopaminergic receptor stimulation appears to play an inhibitory role in the regulation of vasopressin, but not oxytocin secretion in pregnant women in labour.

Adult↗
PubMed1987

Oxytocin reduces metyrapone-induced ACTH secretion in human subjects.

The inhibitory action of oxytocin (OT) on adrenocorticotropin (ACTH) secretion has been disputed. Thus we evaluated the effect of exogenous OT on the elevated blood ACTH levels in normal human subjects. Metyrapone, a blocker of cortisol secretion, was given to enhance ACTH release. This experimental model was chosen because metyrapone-induced ACTH activation depends on diminution of the negative feed-back of cortisol, which is an important physiological mechanism in the control of ACTH secretion. A striking decline in plasma cortisol levels and a 10-fold rise in the mean plasma ACTH concentration was observed within 20 h after the beginning of metyrapone treatment (750 mg orally every 4 h). The administration of OT (2 IU as a i.v. bolus plus 4 IU infused in 2 h) significantly reduced the metyrapone-induced plasma ACTH rise. Since the effect of OT was evident when ACTH secretion was enhanced by a reduced cortisol-dependent negative feed-back, confirmation of the inhibitory action of OT on the ACTH secretory system in man is provided.

Adrenocorticotropic Hormone↗
PubMed1987

Naloxone decreases the inhibiting effect of ethanol on the release of arginine-vasopressin induced by cigarette smoking in man.

In order to establish whether ethanol exerts its inhibiting effect on the nicotine-induced release of arginine-vasopressin (AVP) by interacting with an opioid pathway, six normal volunteers were treated with naloxone (2 or 4 mg as IV bolus, plus 5 or 10 mg infused over 105 minutes) during (2 nonfilter) cigarette smoking and ethanol (50 mL to 110 mL of whiskey) drinking. In addition, control experiments with naloxone, ethanol, or cigarette smoking alone were performed. When given alone, naloxone and ethanol did not modify AVP secretion, whereas nicotine increased plasma AVP levels by about 2.5-fold. This effect was completely blocked by ethanol. In the presence of naloxone, AVP rose only by about 1.7-fold in response to nicotine. Since naloxone only partially reversed the inhibiting effects of ethanol, only a partial involvement of opioid peptides in ethanol action might be supposed. Alternatively, ethanol and naloxone-sensitive opioids might produce their inhibiting effects on AVP rise in response to nicotine through independent pathways.

Adult↗
PubMed1987

Lack of effect of bromocriptine and domperidone on arginine-vasopressin response to insulin-induced hypoglycemia in normal men.

In order to establish whether the arginine-vasopressin (AVP) increase evoked by insulin-induced hypoglycemia is mediated by a dopaminergic pathway, 16 normal men were given an insulin tolerance test (ITT) under basal conditions and after treatment with the dopamine agonist bromocriptine (2.5 mg by mouth) (eight subjects) or the dopamine antagonist domperidone (10 mg i.v.) (eight subjects). In addition, five out of eight subjects in each group were treated with higher doses of bromocriptine (5 mg by mouth) or domperidone (20 mg i.v.). Basal and ITT-stimulated AVP secretion was not modified by the drug treatments, suggesting that dopamine is not involved in the regulation of AVP secretion in response to insulin-induced hypoglycemia.

Adult↗
PubMed1987

Pirenzepine inhibits growth hormone, but not thyrotropin response to thyrotropin-releasing hormone in patients with endogenous depression.

In order to evaluate whether in endogenous depression the anomalous growth hormone (GH) response to thyrotropin-releasing hormone (TRH) is mediated by muscarinic cholinergic receptors, 12 patients were tested with TRH (200 micrograms iv) with and without previous treatment with the muscarinic cholinergic receptor blocker pirenzepine (40 mg iv 10 min before TRH). Control tests with normal saline also were performed. Administration of normal saline did not alter serum GH levels. In contrast, TRH injections significantly increased serum GH concentrations by about three-fold. This response was inhibited by pretreatment with pirenzepine. Another neuroendocrine marker of endogenous depression, the low TSH increase in response to TRH (delta less than or equal to 7 microU/ml), was observed in our patients. Pretreatment with pirenzepine did not modify this response. These data indicate that in patients with endogenous depression a muscarinic cholinergic mechanism is involved in the GH response but not in the TSH response to TRH.

Adult↗
PubMed1987

Evaluation of erythrocyte deformability in pre-menopausal and post-menopausal women.

Whole blood filterability expressed as volume of red blood cells filtered per minute (VRBC) was evaluated in 10 pre-menopausal and 10 post-menopausal women. In addition, blood concentrations of total and high-density lipoprotein (HDL), cholesterol, triglycerides, uric acid, fasting glucose and fibrinogen were measured and correlated with VRBC values. Whole blood filterability was significantly lower in the post-menopausal than in the pre-menopausal women. All the other parameters examined were higher after the menopause, except for HDL-cholesterol levels, which were found to be lower. The VRBC values correlated strongly with fibrinogen, triglyceride and HDL concentrations. These findings indicate that the higher plasma fibrinogen and triglyceride concentrations and the lower HDL-cholesterol levels observed in women after the menopause might be associated with haemorrheological changes. These might be partly responsible for the increased incidence of cardiovascular diseases in post-menopausal women.

Adult↗