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Biomedical subjects

F Boismare

Publications and source records attributed to F Boismare.

At least 55 records · Page 3Linked to original sources
PubMed1983

Effects of oral methoxy-psoralen photochemotherapy (PUVA) on liver function and antipyrin kinetics.

Standard liver function tests and antipyrin kinetics were studied in 19 non-alcoholic patients before and after a four-week PUVA treatment with oral methoxy-psoralen. Whereas liver function remained normal in all subjects, antipyrin clearance was significantly reduced at the end of PUVA therapy. Although the mechanism of this pharmacological effect remains unclarified, these results suggest that there is considerable potential for interactions to occur with other drugs metabolized by the same hepatic pathways (cytochrome P 450) in patients undergoing PUVA therapy.

Adolescent↗
PubMed1983

Potentiation by an alpha-adrenolytic agent, nicergoline, of the cardiac effects of propranolol.

Ten young healthy volunteers were given placebo, propranolol (20 or 40 mg), nicergoline, an alpha blocking agent (30 mg) or the association of nicergoline (15 mg) and propranolol (20 mg) in a randomized double blind study. The results show that nicergoline potentiates the cardiodepressant action of propranolol, whereby the effects of 20 mg become the same as those of 40 mg given alone on cardiac output and myocardial oxygen demand, though the plasma propranolol levels are not changed. We, therefore, propose that nicergoline blocks alpha 1 agonist effects of propranolol, which are usually masked by the greater beta 1 blocking effects but could have clinical and therapeutic relevance.

Adult↗
PubMed1982

Piribedil-induced anti-hypoxic protection in rats.

The action of the dopaminergic agonist, piribedil, on a conditioned avoidance response was studied in normoxic or hypobaric hypoxic rats. This agonist has no effects in normoxia, but induced an anti-hypoxic protection (improvement of learning in hypoxia), antagonised by low doses of pimozide. The mechanism of the anti-hypoxic property seems to be mediated by the stimulation of the postsynaptic dopaminergic receptors, but does not exclude the role of noradrenergic pathways, as shown by the stabilisation of norepinephrine levels during hypoxia after treatment with piribedil.

Air Pressure↗
PubMed1981

Some haemodynamic effects of nicergoline, a new alpha-blocking agent, in the closed-chest anaesthetized dog as compared with nitroprusside and nitroglycerin.

Considering the recent rediscovery of the use of alpha-blocking agents in the treatment of hypertension and heart failure, we have studied the haemodynamic effects of 10-methyl-1,6-dimethyl-ergoline-8 beta-methanol-(5-bromonicotinate (nicergoline, Sermion), a new alpha-blocking ergot derivative, on the closed-chest anesthetized dog. For comparative reasons, the effects of nitroglycerin and nitroprusside were studied on the same model. The doses were adjusted to give an identical decrease in blood pressure after 30 min infusion (nearly 30%). Nicergoline did not change the heart rate, decreased total and femoral arterial resistance, did not change the cardiac output or the femoral flow, as opposed to nitroglycerin which decreased the cardiac output and systolic volume, causing a reflex tachycardia and femoral constriction, confirming its predominantly venous effect. Nitroprusside did not cause tachycardia, and the femoral resistances were increased, though less so than with nitroglycerin. Both nitroglycerin and nitroprusside apparently had no direct effect on myocardial performance, whilst nicergoline seemed to increase the myocardial compliance (by a decrease of the sympathetic tone). This drug merits further attention in that it is readily soluble and can easily be administered i.v., for treatment of acute heart failure, for example.

Anesthesia↗
PubMed1981

Dopaminergic agonists and conditioned avoidance response in normoxic or hypoxic rats.

The actions of four dopaminergic agonists (apomorphine, bromocriptine, amantadine, piribedil) on a conditioned avoidance response were studied in normoxic or hypobaric hypoxic rats. Low doses of agonists have no effects on normoxia, but induce an antihypoxic protection (improvement of learning both in normoxia and hypobaric hypoxia. The possibility of an antihypoxic property induced by dopaminergic post-synaptic receptors stimulation is discussed and seems to be the main receptors stimulation is discussed and seems to be the main phenomenon while action or other non-specific sites seems to be responsible for the high dose-induced impairment of learning and of resistance to hypoxia.

Amantadine↗
PubMed1981

hypobaric hypoxia: central catecholamine levels and cortical PO2 and avoidance response in rats treated with apomorphine.

The learning of a conditioned avoidance response, the catecholamine levels in some cerebral structures, and the evolution of the cortical PO2, were studied under hypobaric hypoxia (300 torr) and under normoxia, in rats treated or not with apomorphine, at the dose of 1 or 10 mg/kg i.p. Apomorphine at 1 mg/kg improves the learning capacity and stabilises the cerebral catecholamine levels under hypoxia; no modification of the evolution of the cortical PO2 during hypoxia was observed between control rats and rats treated with this dose of apomorphine. Apomorphine at 10 mg/kg totally inhibits learning under normoxia or hypoxia. It is therefore possible to suppose that the antihypoxic protective mechanism of low-dose apomorphine is due to a stabilization of the levels of both dopamine and noradrenaline during hypoxia, but not to an increase in the cerebral oxygen availability. These data suggest the clinical possibility of using other dopaminergic stimulating agents for their eventual antihypoxic properties.

Air Pressure↗
PubMed1981

Avoidance learning and mechanism of the protective effect of apomorphine against hypoxia.

We have analyzed a conditioned avoidance response (CAR) in rats, under both normoxia and hypobaric hypoxia (300 torr), to try to elucidate the mechanism of apomorphine's protective effect against hypoxia. The resistance to hypoxia is markedly increased by apomorphine (1 mg/kg i.p.) and, to a lesser degree, by an alpha-adrenergic pre-synaptic (yohimbine 1 mg/kg i.p.) or post-synaptic (phenoxybenzamine 1 mg/kg i.p.) blocker. The anti-hypoxic property of apomorphine is not altered when associated with domperidone (0.5 mg/kg i.p.), a peripheral blocker of the dopaminergic receptors. Resistance to hypoxia is decreased by propranolol (1 mg/kg i.p.) and pimozide (1 mg/kg i.p.). It is not modified by tylciprine (2 mg/kg i.p.) or by metergoline (2.5 mg/kg i.p.), a blocker of the 5-hydroxytryptamine (5 H T) receptors. However, the association of any of the above pharmacological agents with apomorphine destroys apomorphine's anti-hypoxic effect. There has even been shown a positive potentialisation ( i.e. an increase of the inhibitory effect) between apomorphine, hypoxia, and the added drug. This potentialisation is already noticeable under normoxia for the association of each of the drugs with apomorphine. Free alpha, beta adrenergic, cerebral dopaminergic, and serotoninergic receptors and an intact amine metabolic pathway therefore seem required for apomorphine to develop its anti-hypoxic activity.

Animals↗
PubMed1981

Modifications of the dopaminergic receptors sensitivity and learning of normoxic or hypobaric hypoxic rats.

In the present work we attempted to show whether a modification of the sensitivity of the dopaminergic receptors could act on the learning process in hypobaric hypoxia. Acute treatment with 1 mg/kg-1/day-1 pimozide increases the hypoxia-induced deleterious effect on a conditioned avoidance test whilst chronic administration of pimozide improves behavioral performances in hypoxic rats. Chronic treatment with apomorphine does not modify the learning both in normoxic and hypoxic rats in comparison with control rats, while acute treatment induces an anti-hypoxic protection and a fall in total responses (avoidance + escape). A pimozide-induced hypersensitivity (by chronic treatment) or a direct apomorphine-induced stimulation (by acute treatment) of post-synaptic dopaminergic receptors oppose the deleterious effects of hypobaric hypoxia.

Animals↗
PubMed1980

Blockade of the different enzymatic steps in the synthesis of brain amines and memory (CAR) in hypobaric hypoxic rats treated and untreated with L. dopa.

L. Dopa associated with an extracerebral inhibitor of dopadecarboxylase is able to protect the rat against the deleterious effects of hypobaric hypoxia on a conditioned avoidance response. L. Dopa loses its protective effect against hypoxia if tyrosine hydroxylase, dopadecarboxylase, or dopamine beta hydroxylase is previously blocked. L. Dopa's protective effect must therefore be due to an indirect action on the endogenous catecholamine metabolism.

Acoustic Stimulation↗
PubMed1979

[Hemodynamic effects of nicergolin in man at rest and during exertion (author's transl)].

In 10 healthy subjects the injection of 10-methyl-1,6-diemthyl-ergoline-8 beta-methanol-(5-bromonicotinate (nicergoline, Sermion) (5 mg i.v.) caused a permanent decrease in blood pressure. This decrease in blood pressure is due to a rapidly occurring alpha-blocking effect and a secondary central alpha-stimulating effect which did not affect the postural regulating mechanisms of the arterial blood pressure in their function. The bradycardia and the elevation of the systolic volume and of the cardiac output are based on this central effect. After oral administration of 30 mg nicergoline the same modifications appeared but to a lesser extent. If nicergoline was administered in a dosage of 30 mg p.o. 1 h before bicyle exercise (100 W for 5 min), the cardiac output and blood flow in the lower extremities increased and the elevation of the systolic pressure was limited. However, the reactive tachycardia remained at the same level. The metabolic consequences of this administration resulted in an inhibited increase in the concentration of lactic acid in the blood, which is normally caused by this exertion. This favourable metabolic effect can be explained by 1. the initial bradycardia and the decrease in the total peripheral resistance whereby the oxygen consumption of the myocardium is reduced; 2. the peripheral vasodilation.

Adult↗
PubMed1978

Action of cytidine diphosphocholine on functional and hemodynamic effects of cerebral ischemia in cats.

The depression of evoked cortical potentials caused by brief periods of cerebral ischemia is attenuated by prior intracarotid injection of cytidoline (2, 4 or 8 mg/kg). Studies performed in hypercapnic cats suggest that the protection afforded by cytidoline is of metabolic rather than hemodynamic origin. The participation of the central dopaminergic structures by the drug is suggested according to the previous data.

Animals↗
PubMed1978

Biochemical and behavioural effects of hypoxic hypoxia in rats: study of the protection afforded by ergot alkaloids.

The conditioned avoidance response and the cerebral levels of dopamine and noradrenaline have been studied in control rats and in rats submitted to a hypobaric hypoxia. A protection against the effects of hypoxia was induced by both dihydroergocornine (20 microgram/kg) and dihydroergocryptine (100 microgram/kg), and the noradrenaline level did not decrease. This stabilization of cerebral noradrenaline level seems to be the main protection factor observed.

Animals↗