Biomedical subjects

P Chiodera

Publications and source records attributed to P Chiodera.

At least 109 records · Page 6Linked to original sources

PubMed1992

TRH test in alcoholics: relationship of the endocrine results with neuroradiological and neuropsychological findings.

Neuroradiological, neuropsychological and neuroendocrine parameters were evaluated in 20 non-depressed alcoholic men after 4 weeks (N = 11) or after at least 1 year (N = 9) of abstinence from alcohol and in normal men (N = 9). With regard to normal controls, 4-week abstinent alcoholics showed larger lateral and third ventricles, without modification in the number of cerebral sulci, and altered scores of tests evaluating subcortical and frontal function. Furthermore, in these patients the TSH (thyroid stimulating hormone) and PRL (prolactin) responses to thyrotropin releasing hormone were higher than in controls, suggesting a reduced hypothalamic control of TSH and PRL secretion. Taken together, these findings suggest the presence of a frontal-subcortical disorder in alcoholics. Patients who had been abstinent from alcohol for at least 1 year were not distinguishable from controls for neuroradiological, neuropsychological and neuroendocrine findings, suggesting that the alcohol-related brain alterations are reversible after a long period of abstinence.

Adult↗

PubMed1991

Endogenous opioid mediation of somatostatin inhibition of arginine vasopressin release evoked by insulin-induced hypoglycemia in man.

In order to establish whether endogenous opioids play a role in the control of arginine vasopressin (AVP) response to insulin-induced hypoglycemia by interacting with somatostatin (SRIH), seven normal men were submitted to an insulin (0.15 U/kg) tolerance test (ITT) in the presence or absence of naloxone (10 mg in an i.v. bolus), SRIH (4.1 micrograms/min x 90 min) or the combination of the two substances. Plasma AVP concentrations rose significantly during ITT. The AVP response remained unchanged in the presence of naloxone, whereas it was significantly reduced by the treatment with SRIH. When both SRIH and naloxone were given, the hypoglycemia induced AVP rise was similar to that observed in the control test. These results indicate the involvement of naloxone sensitive endogenous opioids in the mechanism underlying SRIH inhibitory action, but not in the mediation of the AVP response to hypoglycemia.

Adult↗

PubMed1991

Reduced ACTH/cortisol responses to naloxone in men with Parkinson's disease.

In order to establish whether the inhibitory control exerted by endogenous opioid peptides on ACTH/cortisol secretion changes in patients affected by Parkinson's disease, ten parkinsonian male subjects and eight age matched normal controls were tested with naloxone (4 mg an i.v. bolus plus 10 mg infused in two hours). In a different occasion all subjects were tested with normal saline. Experiments started at 09.00 h. Plasma ACTH and cortisol concentrations showed a slight physiological decline during saline test in both groups. In the normal controls and in the parkinsonian patients both ACTH and cortisol levels were significantly higher after naloxone administration than during saline test. However, both naloxone induced ACTH and cortisol responses were significantly higher in normal than in parkinsonian subjects. In agreement with the well-known opioid deficiency characterizing the parkinsonian brain, these data show a reduced opioid inhibitory control of ACTH/cortisol secretion in patients with Parkinson's disease.

Adrenocorticotropic Hormone↗

PubMed1991

Oxytocin does not modify the prolactin response to metoclopramide in normal women.

The present study was undertaken in order to establish whether oxytocin (OT) affects the dopaminergic control of PRL secretion in normal women during follicular, periovulatory and luteal phase of their menstrual cycle. For this purpose, 22 normal women were tested with a lower (1 mg) or higher (10 mg) dose of the dopaminergic antagonist metoclopramide (MCP) with or without the concurrent treatment with OT (2 IU injected plus 0.033 IU/min infused for 2 h). Since OT was found unable to modify the effect of either 1 or 10 mg MCP, in additional experiments the same doses of MCP and OT were administered after dopamine (0.04 micrograms/kg/min for 2 h) infusion. Also in these experimental conditions OT failed to modify the PRL response to MCP. These data argue against a role of OT in modulation of the dopaminergic control of PRL secretion in normal women.

Adult↗

PubMed1991

Effect of estrogen or insulin-induced hypoglycemia on plasma oxytocin levels in bulimia and anorexia nervosa.

Plasma oxytocin (OT) levels were measured before and after stimulation with estrogens (1 mg ethynylestradiol orally) or with insulin (0.15 IU/kg)-induced hypoglycemia in seven underweight women with anorexia nervosa, eight normal weight bulimic women, and nine normal controls. Anorectic patients were amenorrhoic; they were tested at their first hospitalization (first tests) and again 8 to 9 weeks later (second tests) when they were eating normally, but were still at a low weight. In addition, anorectic women were tested 16 to 17 weeks after the first test (third tests), when their weight was restored to normal. Normal and bulimic women were tested on the fourth days of normal menstrual cycles. Insulin induced similar hypoglycemic responses in all groups. At each time point of the estrogen tests, plasma estrogen levels were similar in bulimic and normal women, whereas they were significantly lower in anorectic subjects. There were no differences in the basal levels of OT among groups. Both insulin-induced hypoglycemia and estrogen treatment produced striking OT increments in bulimic and control women, without significant differences between groups. During the first tests, no significant increase in plasma OT levels was observed in underweight anorectic women in response to both releasing stimuli. After partial weight recovery, the anorectic women showed a slight, but significant, increase in the OT responses to both insulin-induced hypoglycemia and estrogen administration. Both hypoglycemia- and estrogen-induced OT increases observed during the second tests were significantly lower in underweight anorectic patients than in normal controls. Anorectic subjects regained normal OT responsiveness to both stimuli after complete weight recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Anorexia Nervosa↗

PubMed1991

Reduction of GH response to the GABA-B agonist baclofen in patients with major depression.

In order to establish whether alterations in the GABAergic control of GH secretion occur in male patients with major depression, the GH response to the GABAergic-B agonist baclofen (10 mg PO at 0830h) or to placebo was tested in 9 depressed men and in 10 age- and weight-matched male normal controls. The basal concentrations of GH were significantly lower in the depressed patients (0.87 +/- 0.69 ng/ml) than in the normal controls (1.57 +/- 0.33 ng/ml) (p = 0.011) and were not modified by the administration of placebo. The administration of baclofen induced a striking, significant increase in GH concentrations in the normal controls (mean peak at 90 min = 6.4 +/- 1.5 ng/ml). In contrast, a slight, nonsignificant GH increase occurred in the depressed patients after baclofen (mean peak at 90 min = 1.57 +/- 1.45 ng/ml). The GH response was significantly lower in the depressed than in the control subjects (p less than 0.001). These data indicate the presence of reduced GABAergic control of GH secretion in male depressed patients.

Adult↗

PubMed1991

Luteinizing hormone responses to gonadotropin-releasing hormone and naloxone in menstruating women with type I diabetes of different duration.

Luteinizing hormone (LH) responses to gonadotropin-releasing hormone (GnRH) (100 micrograms injected intravenously (IV)) or naloxone (4 mg injected plus 8 mg infused in 2 hours IV) were evaluated in 29 women with insulin-dependent diabetes mellitus (IDDM) (duration, group I (n = 15): less than 10 years, range 3 to 9 years; group II (n = 14): greater than 10 years, range 11 to 20 years) and in 15 normal controls, on the 22nd days of normal menstrual cycles. Both GnRH- and naloxone-induced LH responses were similar in group I diabetics and normal controls, whereas they were significantly lower in group II than in group I diabetics or normal controls. Positive correlations were found between LH responses to GnRH and naloxone, whereas negative correlations were observed between maximal LH peaks in response to GnRH or naloxone and duration of diabetes. These data indicate that a hypothalamic pituitary disorder affects LH secretion with time after the onset of IDDM.

Adult↗

PubMed1991

Reduction of baclofen-, but not sodium valproate-induced growth hormone release in type I diabetic men.

The effects of sodium valproate (a drug enhancing endogenous gamma aminobutyric acid (GABA)-ergic activity) and of the GABA analog baclofen (a GABA B receptor agonist) on serum GH levels was tested in 8 type I diabetic men and 8 normal controls. Sodium valproate (800 mg) or baclofen (10 mg) were given by mouth at 08.30 h on the experimental day. Control tests with a placebo were performed on different occasions. Basal GH levels were similar in controls and diabetic patients. Sodium valproate induced a 7 fold increase in serum GH concentrations in both groups. In contrast, baclofen-induced GH rise was significantly higher in normal controls (mean peak was 3.4 times higher than baseline) than in diabetic patients (mean peak was only 2.1 times higher than basal value). Serum GH levels did not change after placebo administration in any groups. These data suggest the presence of diabetes-induced alterations of a GABAergic pathway mediated by B receptors in the control of GH secretion. Alternatively, the data might indicate a change in diabetic men of other baclofen-sensitive neurotransmissions, different from GABA.

Adult↗

PubMed1991

Abnormal arginine vasopressin response to cigarette smoking and metoclopramide (but not to insulin-induced hypoglycemia) in elderly subjects.

Aging is known to reduce arginine vasopressin (AVP) response to volumetric stimulations and to increase AVP responses to osmotic stimuli and to administration of metoclopramide (MCP). In order to gain a better insight into the effect of age on AVP secretion, we evaluated AVP responses to cigarette smoking, MCP, and insulin-induced hypoglycemia in 30 male subjects aged 22-81 and divided into 3 groups by age. Basal AVP concentrations were similar in all groups. The AVP response during the insulin tolerance test had a similar pattern and magnitude (2.5-fold increase) in all groups. AVP responses to MCP and cigarette smoking were similar in the two younger groups, with plasma AVP levels increased 2 times by MCP and 2.5 times by cigarette smoking. In contrast, both MCP- and cigarette smoking-induced AVP rises were significantly higher in the oldest group, where plasma AVP concentrations increased 2.5 times after MCP and 3.25 times after smoking. When data of the MCP and cigarette smoking tests were combined, regression analyses showed a significant positive correlation between AVP peak responses to MCP and cigarette smoking in the oldest subjects. These data show that elderly humans have increased AVP responses not only to MCP but also to cigarette smoking, suggesting a common disorder for both alterations. In contrast, the lack of age-related changes in AVP response during the insulin tolerance test demonstrates that the mechanism underlying the AVP response to hypoglycemia is not affected by aging.

Adult↗

PubMed1991

Restoration of normal growth hormone responsiveness to GHRH in normal aged men by infusion of low amounts of theophylline.

In order to establish whether the age-related reduced growth hormone (GH) responsiveness to GH-releasing hormone (GHRH) could be improved by treatment with low amounts of theophylline, a drug mainly acting through cyclic adenosine 3', 5'-monophosphate (cAMP), and calcium-mediated mechanisms, eight adult subjects (aged 20-37) and eight elderly men (aged 64-79) were tested with GHRH (50 micrograms in an iv bolus), theophylline (1.67 mg/min for 3 h), or the combination of both drugs. The GH response to GHRH was significantly lower in the older than in the younger group (mean peaks were 4.5 and 7.5 times higher than baseline, respectively). Theophylline did not change basal GH levels in any subjects and GHRH-induced GH rise in the younger group, whereas it restored normal GH responses to GHRH in the older subjects (mean peak responses were eight times higher than baseline in both groups). These data show that in elderly subjects the mechanism underlying the GHRH-induced GH secretion may be fully activated by GHRH during treatment with low amounts of theophylline.

Adult↗

PubMed1991

Naloxone increases the angiotensin II stimulated rise of arginine vasopressin and oxytocin secretion in man.

The effect of systemic angiotensin II (ANG II) administration on the posterior pituitary function was investigated in normal men. In addition, the role of endogenous opioids in the control of arginine vasopressin (AVP) and/or oxytocin (OT) responses to ANG II was evaluated with the administration of the opioid antagonist naloxone. ANG II (i.v. infusion for 60 min of successively increasing doses of 4, 8 and 16 ng/kg min; each dose for 20 min) was given to 7 normal men, alone or together with naloxone (10 or 20 mg injected i.v. just before ANG II infusion). In all subjects, control experiments with naloxone (10 or 20 mg) alone were also performed. ANG II induced a significant increase in plasma concentrations of AVP and OT. The AVP and OT responses to ANG II had a similar magnitude and followed a similar pattern. The mean peak levels of both hormones were reached at 60 min after the beginning of ANG II infusion. The administration of 10 or 20 mg naloxone alone did not modify the circulating concentrations of AVP and OT. The pretreatment with naloxone significantly increased both ANG II-induced AVP and OT increases twofold, without changing the time course and the secretory pattern of the hormonal responses. These data demonstrate that systemic administration of ANG II in man induces similar simultaneous increments in plasma levels of both AVP and OT. Furthermore, these data suggest the involvement of a naloxone-sensitive opioid mechanism in the regulation of both AVP and OT responses to ANG II in man.

Adult↗

PubMed1991

Relationship between plasma profiles of oxytocin and adrenocorticotropic hormone during suckling or breast stimulation in women.

Oxytocin (OT) administration has been shown to inhibit adrenocorticotropic hormone (ACTH)/cortisol secretion in several experimental conditions. In the present study, the plasma OT responses to suckling in 7 lactating women or to mechanical breast stimulation in 6 normally menstruating women (experimental tests) or to sham stimuli in the same subjects (control tests) were measured and correlated with the simultaneous changes in plasma ACTH/cortisol levels. All women showed similar basal levels of OT, ACTH and cortisol, which remained unmodified after sham stimulation. In contrast, both suckling and breast stimulation produced a significant increase in plasma OT levels and a significant decrease in plasma ACTH concentrations. When OT and ACTH data were considered together, a significant negative correlation was found between the OT increase and the simultaneous ACTH decline. Plasma cortisol levels were lower during suckling or breast stimulation than in control conditions. These data show an inverse relationship between plasma OT and ACTH levels during suckling and breast stimulation in humans, suggesting an inhibitory influence of OT on ACTH/cortisol secretion in a physiological condition.

Adrenocorticotropic Hormone↗

PubMed1991

Different effects of the GABAergic agent sodium valproate on the oxytocin responses to angiotensin II and insulin-induced hypoglycemia in normal men.

The present study was performed in order to establish whether angiotensin II (ANG II) and/or insulin-induced hypoglycemia exert their oxytocin (OT)-releasing effects by interacting with a GABAergic pathway. For this purpose, in 14 normal men the OT responses to ANG II (infusion for 60 min of successively increasing doses of 4, 8 and 16 ng/kg.min, each dose for 20 min; n = 7) or to insulin (0.15 IU/kg)-induced hypoglycemia (n = 7) were evaluated with or without previous treatment with the GABAergic agonist sodium valproate (600 mg in 3 divided doses, p.o.). In all subjects insulin produced a similar hypoglycemic response regardless of sodium valproate administration. Both ANG II and insulin-induced hypoglycemia produced significant increases in plasma OT levels (mean peaks were about 60% higher than baseline). The pretreatment with sodium valproate was unable to change the OT response to hypoglycemia, whereas it abolished the ANG-II-induced OT rise. These data suggest that in man a GABAergic mechanism is involved in the regulation of the OT response to ANG II, but not in the mediation of poglycemia-induced OT release.

Adult↗

PubMed1991

Restoration of normal gonadotropin responses to naloxone by chronic bromocriptine treatment in elderly men.

Naloxone is unable to stimulate FSH and LH secretion in elderly men, suggesting a reduced endogenous opioid control of gonadotropin secretion in senescence. In the present study, we examined whether in elderly men a chronic dopaminergic stimulation with bromocriptine (5 mg/day for 7 days) modifies the gonadotropin response to naloxone (4 mg as an i.v. bolus plus 10 mg infused in 2 h). Eleven younger men (group 1, 22-40 years old) participated as controls. Twenty-two elderly men were selected from a larger population and were divided into two groups: subjects with compensated gonadal failure (normal blood testosterone and elevated gonadotropin concentrations; group 2, n = 11; 62-80 years old) and men with normal gonadal function (normal blood testosterone and gonadotropin levels; group 3, n = 11; 61-82 years old). Naloxone induced a striking LH and a slight but significant FSH increase in group 1, but was unable to change serum gonadotropin concentrations in elderly subjects of both groups 2 and 3. When experiments were repeated after bromocriptine treatment, no significant differences in LH and FSH responses to naloxone were observed in the younger subjects. On the other hand, bromocriptine restored significant gonadotropin responses to naloxone in elderly men. In fact, after bromocriptine, naloxone-induced FSH and LH increments in groups 2 and 3 were indistinguishable from those observed in group 1. These data suggest that in men age-related dopaminergic alterations may underlie the defective endogenous opioid control of gonadotropin secretion.

Adult↗

PubMed1991

Failure of the gamma-aminobutyric acid (GABA) derivative, baclofen, to stimulate growth hormone secretion in Parkinson's disease.

In order to evaluate whether the stimulating effect of GABA on growth hormone (GH) secretion changes in patients affected by Parkinson's disease, ten male parkinsonian patients and ten age matched normal controls were tested with the GABA derivative and GABAergic agent Baclofen (10 mg in a single oral administration at 09.00 h) (experimental test). In a different occasion, normal men and parkinsonian patients were tested with a placebo (control test). Basal GH levels were similar in normal controls and parkinsonian patients and remained unmodified during the control test. Plasma GH levels rose three times within 120 min after the administration of baclofen in the normal subjects. In contrast, plasma GH concentrations remained unmodified after baclofen treatment in the parkinsonian patients. In agreement with previous reports in the literature showing alterations of GABAergic neurotransmission in the parkinsonian brain, these data show a reduced GABAergic control of GH secretion in patients with Parkinson's disease.

Aged↗

PubMed1990

Increase by naloxone of arginine vasopressin and oxytocin responses to insulin-induced hypoglycemia in obese men.

The present study was carried out to establish whether the low arginine vasopressin (AVP) and oxytocin (OT) responses to insulin-induced hypoglycemia observed in obese men was due to alteration of the opioid control of posterior pituitary function. For this purpose, the AVP and OT releasing effect of insulin (0.15 IU/kg bw)--induced hypoglycemia was tested in eight normal weight men and in 10 age-matched obese subjects, without and with the previous treatment with the specific opioid receptor antagonist naloxone (3 mg in an iv bolus). In a control study, naloxone was given alone to the same subjects. Obese men showed similar basal glucose, AVP and OT levels, which remained unmodified after treatment with naloxone alone. Insulin induced a similar decrement of blood glucose levels in all subjects, with a nadir at 30 min. Plasma levels of AVP and OT rose strikingly in normal and obese subjects with mean peak responses at 30 min for AVP and at 45 min for OT. However, both AVP and OT responses were significantly lower in obese than in control subjects. Pretreatment with naloxone did not modify the AVP and OT responses to hypoglycemia in normal weight subjects, whereas it significantly enhanced both hormonal responses in obese subjects. In the presence of naloxone normal controls and obese subjects showed similar responses of both AVP and OT to hypoglycemia. These data indicate that an abnormal activity of endogenous opioids might account for the hypothalamic posterior pituitary dysfunction, which is responsible for the low AVP and OT responses to insulin-induced hypoglycemia in obesity.

Adult↗

PubMed1990

Effect of obesity and weight loss on arginine vasopressin response to metoclopramide and nicotine from cigarette smoking.

We have previously reported an impaired arginine vasopressin (AVP) response to insulin-induced hypoglycemia in obese men, suggesting a hypothalamic-posterior pituitary disorder in obesity. In the present study, we examined the AVP response to other releasing stimuli with a central site of action. The AVP response of 10 obese men to metoclopramide (MCP) or nicotine inhaled with cigarette smoking was compared with that obtained in eight sex- and age-matched controls. The AVP increase during nicotine and MCP tests were significantly lower in the obese patients than in the normal controls. Obese men were restudied after substantial weight loss. The AVP response to nicotine and MCP administration was significantly higher than before slimming and did not differ from that observed in the normal weight subjects. These results demonstrate obesity-related alterations in the AVP responsiveness to nicotine inhaled with cigarette smoking and MCP, supporting the hypothesis for a hypothalamic-posterior pituitary disorder in obesity.

Adult↗

PubMed1990

Luteinizing hormone and cortisol responses to naloxone in normal weight women with bulimia.

The present study was undertaken in order to establish whether alterations in the endogenous opioid control of luteinizing hormone (LH) and ACTH/cortisol secretion occur in bulimic women with normal body weight and normal menstrual cycles. For this purpose, the capability of the opioid antagonist naloxone (4 mg injected as an intravenous bolus at time 0, plus 10 mg infused over 2 hr) to increase the circulating levels of LH and cortisol was tested in nine bulimic women and in nine age- and weight-matched normal controls. All women were tested on the 22nd day of a normal menstrual cycle. Two days later, a control test with normal saline (NaCl 0.9%) instead of naloxone was performed. The basal levels of LH and cortisol were similar in the bulimic and normal subjects and were not modified by the administration of normal saline. In contrast, the administration of naloxone significantly increased plasma LH and cortisol levels in all subjects, with peak LH responses at 30 min and peak cortisol responses at 60 min. The naloxone-induced LH and cortisol increases were significantly higher in the bulimic women than in the normal controls. These data indicate the presence of an increased opioid inhibitory tone in the control of LH and ACTH/cortisol secretion in normal weight bulimic women with normal menstrual cycles.

Adult↗