[Electrocardiographic changes in myocardial damage; effect of treatment with nifedipine].
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Biomedical subjects
Publications and source records attributed to S Gentile.
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A sensitive radioenzymatic assay for the simultaneous determination of phenylethylamine, phenylethanolamine, tyramine and octopamine in plasma samples is reported. After extraction with ethanol, the amines are subjected to enzymatic N-methylation with labelled S-adenosylmethionine, preceded in the case of phenylethylamine and of tyramine, by an enzyme-catalyzed beta-hydroxylation step. The procedure is completed by extraction with toluene containing different amounts of isoamylalcohol, followed by controlled evaporation of the solvent. A generalized and highly significant increase in the concentration of all the four amines was found in plasma samples from patients suffering from hepatic encephalopathy.
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The present study was aimed at investigating the effect of metergoline, a powerful and long-lasting antiserotoninergic agent, on insulin responses to glucose and arginine in adult-onset diabetic subjects. The repeated administration of this agent (10 mg daily for two days plus a 4 mg dose 1 hour before the post-treatment test) or placebo did not influence acute insulin response to intravenous glucose (20 g), total insulin secretion or glucose disappearance rates. Similarly, plasma glucose and insulin levels following arginine (30 g perfused over a period of 40 min) were similar before and after metergoline treatment. These results do not support the hypothesis that an endogenous monoamine mechanism plays an important part in defective insulin secretion in human non insulin-dependent diabetes mellitus.
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Beta-adrenergic receptors from submandibular glands of mice were studied by equilibrium binding experiments. Due to the fact that some discrepancies were previously observed among different author data, we compared two methods for non specific binding substruction, that represents the major source of errors in such experiments. Data were obtained strongly suggesting the presence of multiple population of binding sites and/or negative cooperativity.
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The effect of nifedipine, a calcium antagonist, on carbohydrate metabolism and insulin secretion was evaluated in patients who required treatment with this drug. 20 subjects underwent two oral glucose tolerance tests (100 g), one under basal conditions, and the other after ten days of treatment with nifedipine 30 mg/day by mouth, in three divided doses. 10 subjects had normal glucose tolerance; in them nifedipine administration reduced the insulin response to oral glucose in the first 60 min, but improved glucose tolerance. The other 10 subjects had impaired glucose tolerance and nifedipine treatment resulted in a further reduction both of insulin secretion and glucose tolerance. No such effects were seen in the placebo (weight- and disease-matched) group. The mechanism by which nifedipine influences carbohydrate metabolism and insulin secretion is discussed.
In order to asses potential interactions between somatostatin and prostaglandins during regulation of insulin secretion in vivo, in the present investigation we studied the effect of acetylsalicylic acid, an inhibitor of endogenous PG synthesis, on somatostatin-mediated inhibition of glucose-induced insulin secretion in normal man. Acute insulin response (mean change 3'-10') to glucose was almost completely suppressed by somatostatin (500 microgram/h) and glucose utilization was decreased. These somatostatin-induced changes failed to be eliminated by a concurrent infusion of acetylsalicylic acid (40 mg/min). This last drug, when infused alone, increased both the acute insulin response to glucose and glucose tolerance. These results speak against the involvement of PGs in the mediation of somatostatin-induced suppression of insulin secretion.
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Ten healthy subjects have been given before and after treatment with phenobarbital the following intravenous charges: a) nicotinic acid; b) rifamicyn-SV; c) simultaneous administration of the two drugs. Along with confirmatory evidence of the wellknown increase in bilirubinaemia (prevalently unconjugated), we have observed phenobarbital to attempts partially yet significantly that effect. On the base of direct experience on rat liver, we hypothise phenobarbital to increase the pool of the Y protein carrying cholephilic organic anions into the hepatocytes.
We have studied plasmatic half-life of R-SV administered alone and in association with nicotinic acid, before and after treatment with phenobarbital, in 10 normobilirubinaemic subjects and in 10 patients Gilbert's syndrome, used like controls. Ouer results confirm the existence of some alterations of drug-metabolism produced by associated administration of other drugs, in both healthy and hyperbilirubinaemic subjects, and in these one even more.
The influence of treatment with allopurinol (5 mg/kg/die for 15 days) on T/2 of tolbutamide and rifomycin-SV intravenously administered, has been studied in 10 healthy volunteers. We have observed reduction of T/2 of tolbutamide and, on the contrary, prolongation of T/2 of rifamycin-SV. Tolbutamide behaviour was unexpected, considering that other Authors had previously found inhibition of metabolic degradation of other drugs metabolized by the microsomal enzymes. We conclude that data concerning the influence of a drug (in our case, allopurinol) on the metabolism of another drug cannot always authorize general deduction and previsions regarding the metabolic interferences on the pharmacokinetics of other substances.
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Fourteen cases of vertex epidural hematomas encountered in patients admitted over a 12-year period (1964-1976) at the University of Genoa Neurosurgical Clinic are presented. Special emphasis is put on the large number of cases (nine) without a free interval. Clinical and neuroradiological findings, treatment and results are reported. A clinical classification of this traumatic pathology according to the epidural hematoma classification of Pecker et al is proposed.