Biomedical subjects
Publications and source records attributed to J Duhault.
Long-term administration of fenfluarmine induced a decrease of brain 5-HT to the same extent as did an acute dose. 48 h after drug withdrawal, the brain serotonin level returned to the control value. The present study provides evidence to suggest that a degenerative lesion of 5-HT neurons is not involved in fenfluramine activity.
Diabetic microangiopathy is a degenerative process specific to diabetes. Metabolic theory holds that the metabolic defect predisposes to vascular abnormalities, but other theory suggests that microangiopathy and metabolic disorders are of different origin. Metabolic and ultrastructural modifications in kidney and retina are reviewed. Human and animal studies suggest a specific organ response to fortuitous association of several factors leading to microvascular disease.
A series of phenylisopropylamine derivatives are compared with the correspondent beta-methoxy- and beta-hydroxy-phenethylamine compounds. Unlike amphetamine, the beta-methoxy phenethylamine has no anorectic activity. This property appears only with the introduction of a CF3 group on the benzene nucleus. The racemic N-alkyl derivatives are more active than the racemic or even the levorotatory N-benzyl compound. The beta-hydroxy-phenethylamines are devoid of anorectic activity.
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Thickening of the basement membrane and deposition of collagen-like substances in vascular lesions are well-known findings in diabetes mellitus, suggesting altered metabolism of glycoproteins. Glomerular glucosyltransferase activity were measured in normal and diabetic rats. Enzymic activity in diabetic animals did not differ from control. Another mechanism must be involved in the thickening of the B.M., such as increased production of hydroxylysine-rich peptides or decreased breakdown of B.M. materials.
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1-Phenethyl-4-hydroxy-salicylamido-4-methylpiperidine-hydrochloride (S 1592) markedly inhibits coughing induced in laboratory animals by chemical or mechanical irritation of respiratory tract or by electrical stimulation of the superior laryngeal nerve. The drug has low acute toxicity in mice and rats. The new compound possesses bronchodilating and antianaphylactic properties and does not affect gastrointestinal propulsion. Cardiovascular effects are absent.
Platelet aggregates were formed in flowing blood by infusing ADP in the carotid artery of the dog. Under fluorographic examination, these aggregates were seen to lodge in retina vessels. Previous administration of gliclazide helped maintain normal retina circulation.
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Both fenfluramine and de-ethylated fenfluramine decrease the brain stores of 5-hydroxytryptamine (5-HT). As the fenfluramine metabolite is present in the brain of the rat after fenfluramine injection, it could be suggested that the depletion of brain 5-HT elicited by fenfluramine is mediated by its metabolite. Comparative studies on 5-HT lowering effects and drug brain levels, indicate a primary effect of fenfluramine, following by the rising involvement of the de-ethylated compound in the sustained effect.
As it is well-known, fenfluramine produces anorexia and decrease in brain 5-hydroxytryptamine (5-HT). As it has been suggested that the anorectic effect of fenfluramine may be due to a release of brain 5-HT, we have examined the influence of several drugs active on 5-HT mechanisms and metabolism, on the anorexigenic activity of fenfluramine. These studies were made in relationship with the depletion of 5-HT levels and the concentration of brain fenfluramine or m-trifluoromethyl-isopropylamine. The results have confirmed the involvement of a tryptaminergic mechanism in fenfluramine anorexia and suggest the hypothesis that fenfluramine itself can interfere with the serotoninergic system in the brain (stimulation of tryptaminergic neurons directly).
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