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Biomedical subjects

G Faucon

Publications and source records attributed to G Faucon.

At least 91 records · Page 5Linked to original sources
PubMed1980

Effects of isoproterenol on the metabolism of normal and ischemic heart.

A study has been made of the simultaneous evolution of cardiac activity and metabolism in the dog heart in situ, during the perfusion of isoproterenol in a dose comparable to therapeutic doses (1 micrograms x kg-1 x min-1, 30 min). A total cardiopulmonary by-pass system allowed of taking the repeated myocardial tissue samples necessary for the determination of the main energetic substrate and high-energy phosphate content. Samples were taken from subendocardial and subepicardial layers separately. The acceleration of heart rate due to isoproterenol was quickly regressive but, in the well-irrigated heart, the drug elicited a rapid fall in glycogen content and a considerable rise in lactate content, a slower reduction in free fatty acid concentration restricted to the subendocardial layer, and no significant variation of creatine phosphate or ATP. In the ischemic heart, isoproterenol aggravated the glycolysis disturbances without completely losing its effects on lipolysis when the ischemia was not too marked.

Adenosine Triphosphate↗
PubMed1979

Study of thioridazine cardiotoxic effects by means of His bundle activity recording.

The effect of thioridazine on sinusal automaticity, myocardial excitability and auriculoventricular conduction have been studied in dogs by measuring the spontaneous heart rate, the effective refractory period of the atrial contractile tissue, the time of auriculonodal and infrahisian conduction. Chloralose anaesthetized dogs were administered 10 mg/kg thioridazine hydrochloride via intravenous route. While sinusal automaticity was not altered, conduction times were prolonged in the suprahisian and mainly the infrahisian part and the atrial refractory period increased. These effects are related to quinidine-like properties and consistent with cardiotoxic effects previously reported in clinical practice.

Animals↗
PubMed1979

[Influence of nicergoline on the cerebral blood flow and alpha-sympatholytical properties (author's transl)].

The cerebral vasodilatory effect of 10-methoxy-1,6-dimethyl-ergoline-8 beta-methanol-(5-bromonicotinate) (nicergoline, Sermion) was examined by recording the cardiac output of the vertebral artery in the dog. As from a dosage of 25 micrograms/kg nicergoline increases permanently the cardiac output to a normal or nearly normal level which had been decreased by phenylephrine reducing the increased local vascular resistance. The alpha-sympatholytical properties of nicergoline were more precisely proved by reducing the reactive increase in blood pressure after epinephrine and norepinephrine (3 micrograms/kg) by administration of nicergoline in 3 doses (25, 50 and 100 micrograms/kg). The same method was used with phentalamine in dosages of 125, 250 and 500 micrograms/kg. The statistical comparison of the results obtained with both substances shows that the ratio of equiactive doses is about 3:1 in favour of nicergoline.

Adrenergic alpha-Antagonists↗
PubMed1979

Myocardial biochemical modifications induced by theophylline with reference to its value as antianginal drug.

Theophylline-induced variations of cardiac metabolism have been investigated by determining concentrations of various energetic substrates and of high-energy phosphates in myocardial tissue, the repeated sampling of myocardium being made possible by an extracorporal circulation system. When administered in therapeutic, or even slightly higher doses, theophylline does not modify triglyceride, glycerol and free fatty acid content or phosphocreatine and ATP content in subepicardial and subendocardial layers, but it does lower glycogen and raise lactate concentration. Consequently, the changes in anaerobic glycolysis due to myocardial ischemia may be enhanced if, as is probably the case, theophylline fails to restore the supply of oxygen.

Angina Pectoris↗
PubMed1979

[Effect of levomepromazine on atrioventricular conduction tissue (author's transl)].

The effect of levomepromazine on sinusal automaticity, myocardial excitability and auriculoventricular conduction have been studied in dogs by measuring the spontaneous heart rate, the effective refractory period of the conduction system, the time of auriculonodal and infrahisian conduction. Chloralose-anaesthetized dogs were administered 5 mg/kg levomepromazine via IV route and 10 mg/kg one hour later. While sinusal automaticity is never altered, the other parameters studied were modified only when high doses were used. Therefore these quinidine-like effects are very unlikely to come up even following suicidal massive ingestion of levomepromazine.

Animals↗
PubMed1978

Relationship between atrial and ventricular rates of fibrillation and cardiac contractile tissue effective refractory periods in the dog.

1 During total cardiopulmonary bypass, acetylcholine-, isoprenaline-, ouabain- and quinidine-induced variations in the atrial and ventricular rates of fibrillation were studied and compared with the variations in effective refractory periods (ERP) of atrial and ventricular contractile tissue obtained under the same experimental conditions. 2 Acetylcholine significantly shortened the ERP and accelerated the rate of fibrillation in the atrium but did not provoke any change in ventricular tissue. A parallel decrease in atrial and ventricular ERP and a parallel increase in atrial and ventricular rates of fibrillation were observed with isoprenaline. 3 Ouabain exerted a biphasic effect on the atrium, with an initial decrease in the ERP and an initial acceleration of the rate of fibrillation. It produced only a slight decrease in the ventricular ERP and no significant variation in the ventricular rate of fibrillation. 4 Quinidine induced a greater increase in the ERP and a greater slowing of the rate of fibrillation in the atrium than in the ventricle. 5 The variations in percentage change of refractoriness and rate of fibrillation were strictly correlated: r = 0.89 (P less than 0.001); the equation of the regression line was y = --0.86 x --2.98.

Acetylcholine↗
PubMed1977

Influence of acetylcholine, isoproterenol, quinidine and ouabain on effective refractory periods of atrial and ventricular myocardium in the dog.

Acetylcholine-, isoproterenol-, quinidine- and ouabain-induced variations of the effective refractory periods (E.R.P.) of the non-specialized atrial and ventricular tissue have been explored in the dog by the extra-stimulus method during total cardiopulmonary by-pass. Acetylcholine significantly shortens the E.R.P. of atrial fibers, but does not provoke any change in the ventricular tissue, whereas a parallel decrease of atrial and ventricular E.R.P. is noted with isoproterenol. Quinidine induces a larger increase of the E.R.P. in the atrium than in the ventricle. The ouabain-induced shortening of the E.R.P. in the atrium is more marked than in the ventricle but is followed by a secondary increase which depends on both time after injection and dose. Hypotheses about the mechanisms of these effects, their importance in fibrillation and their relation to clinical uses are discussed.

Acetylcholine↗