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Biomedical subjects

E Marmo

Publications and source records attributed to E Marmo.

At least 19 recordsLinked to original sources
PubMed1979

Prostaglandin F2 alpha and cardiovascular system: review of studies conducted in dogs.

The study was designed to investigate the effect of PGF2 alpha on the arterial, cardiac and venous system and the respiration of dogs. PGF2 alpha was administered in single, graded doses as well as by i.v. perfusion. In addition, PGF2 alpha was given intra-arterially into the common carotid artery, by inhalation and by infiltration into the barosensitive zone of the carotid sinus. The interaction by drugs acting on ganglia, the catecholamine stores and the muscarinic, histaminergic, serotonergic, adrenergic and purinergic junctions, and by drugs with depressive effects at the prostaglandin receptors, also were studied. We have shown that PGF2 alpha exhibits direct, reflexes and modulator effects.

Animals↗
PubMed1979

Antagonism of prostaglandin E1 and E2 fever by catecholamines.

Antagonism of PGE1 and PGE2 fever by catecholamines in adult fowls was studied by infusing these substances into the brain. PGE1 and PGE2, given into the third cerebral ventricle or into the hypothalamus, produced an immediate, intense and long-lasting increase in body temperature. Noradrenaline and alpha-methylnoradrenaline infused into the hypothalamus or into the third cerebral ventricle during the fever peak were able to antagonize it and to revert the hyperthermic effect into an hypothermic effect. The possible modes of action of PG's and relations with catecholaminergic neurons in the hypothalamus are discussed.

Animals↗
PubMed1978

Central cardiovascular effects of clonidine and another imidazoline derivative ST [600] in adult fowls.

In adult fowls (Gallus domesticus) with cannulae stereotaxically implanted into the III cerebral ventricle and into the hypothalamus, the effects of clonidine and another imidazoline derivative (St 600) were studied on arterial blood pressure and heart rate. It has been shown that clonidine and St 600 administration into the III ventricle or into the hypothalamus produced an immediate profound and long lasting decrease in blood pressure and heart rate. Contrary to the intravenous administration, this response was not preceded by an initial rise in blood pressure. On an equimolar basis St 600 appeared to be at least one-tenth as potent as clonidine. Prior intraventricular administration of alpha-adrenoceptor blocking agents, phentolamine and phenoxybenzamine, prevented changes in cardiovascular effects following intrahypothalamic infusion of clonidine and St 600. In conclusion, present experiments indicate that in fowls the hypothalamus represents the site or sites through which hypotension and bradycardia evoked by clonidine and related compounds are mediated.

Animals↗