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Biomedical subjects

C Davoli

Publications and source records attributed to C Davoli.

At least 37 records · Page 2Linked to original sources

[Dyspeptic syndrome in heart diseases].

Many investigations have ascertained the relation between dyspepsia and diseases or disorders of gastrointestinal tract; on the contrary, the topics concerning the dyspeptic syndrome during acute cardiac disorders are very few. For this reason, Authors studied the upper tract of digestive apparatus in some patients affected with congestive heart failure and ischemic heart disease. Data have showed alterations of motility in esophagus, stomach and duodenum in every patient and lesions of gastric mucous membrane in more than half of them.

Adult↗

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↗

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↗

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↗

Nicotinic and M1-, M2-muscarinic cholinergic control of ACTH response to insulin-induced hypoglycaemia in man.

The possible mediation of muscarinic and/or nicotinic-cholinergic receptors in the response of ACTH to insulin-induced hypoglycaemia was evaluated in 18 normal men. Subjects were tested with the insulin (0.15 U/kg) tolerance test (ITT) in basal conditions and in the presence of the M1- and M2-muscarinic antagonist atropine (600 micrograms iv just before insulin injection (time 0) plus 600 micrograms 20 min later in 6 subjects) or the M1-muscarinic receptor blocker pirenzepine (40 mg iv 10 min before ITT or 20 mg at time 0 plus 30 mg at time 20 in 6 subjects). The remaining 6 men were treated with the nicotinic receptor antagonist trimethaphan (0.3 mg/min x 30 min before ITT). ACTH rose 4.7 times in response to hypoglycaemia. The ACTH response to hypoglycaemia did not change after pirenzepine administration, whereas it was significantly increased by atropine and decreased by trimethaphan treatment. These data indicate that nicotinic and muscarinic (M2 but not M1) receptors participate in a different manner in the regulation of the hypoglycaemia-induced ACTH release.

Adrenocorticotropic Hormone↗

Thyrotropin-releasing hormone does not inhibit lysine vasopressin-induced growth hormone secretion in normal men.

In order to establish whether thyrotropin-releasing hormone (TRH) inhibits lysine-vasopressin (LVP)-induced growth hormone (GH) release, six normal men were tested with LVP alone or in combination with TRH. LVP strikingly increased serum GH levels; this response was not altered by TRH. These results indicate that in man TRH is not involved in the control of GH secretion in response to LVP.

Adult↗

Sporadic acute non-A non-B hepatitis complicated by aplastic anemia.

A 19-year-old woman developed acute jaundice and abnormal liver tests showing acute viral hepatitis, presumably non-A non-B. The viral hepatitis, on the 4th day after admission, was complicated by aplastic anemia. Therapy with hydrocortisone promptly instituted was ineffective and a bone marrow transplantation was not possible because we could not find a compatible donor. Sixty-five days after admission the patient died of infection by Candida tropicalis. Postmortem examination showed total medullary aplasia with massive impoverishment of all the lymphatic structures and multiple fungal infarctions in the myocardium, lungs, spleen, kidneys, and liver.

Acute Disease↗

The isoelectric focusing of human thyroglobulin.

The isoelectric focusing of human thyroglobulin has been studied on slab gels. Three bands, focusing between pH 4.4 and 4.7, are observed. Deglycosylation of thyroglobulin does not affect the distribution of focused bands, but increases the pH range of focusing slightly. Native thyroglobulin and its half-sized subunit show the same distribution of isoelectric bands. Refocusing of one band results in the appearance of the three original bands. It appears that soluble complexes of thyroglobulin with ampholyte account for the apparent heterogeneity observed on isoelectric focusing.

Ampholyte Mixtures↗

Immunoreactive properties of anti-thyroglobulin autoantibodies isolated by affinity chromatography from human thyroiditis serum.

A Sepharose-coupled 19S human thyroglobulin has been used as an immunoadsorbent to isolate anti-thyroglobulin autoantibodies and to evaluate the antigen-antibody interactions. With the system proposed a high yield of active antibody molecules was obtained. It is possible to evaluate both the soluble and precipitating 'immunological interactions', thus avoiding the use of the double antibody technique.

Antigen-Antibody Reactions↗