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Biomedical subjects

G Faucon

Publications and source records attributed to G Faucon.

At least 163 records · Page 9Linked to original sources
PubMedDate not supplied

[Comparison of myocardial metabolic effects of in subendocardial and subepicardial layers ischaemia and beta-adrenergic stimulation (author's transl)].

The influence of beta-adrenergic stimulation on myocardium carbohydrate and lipid metabolism has been compared with the influence of ischemia in anesthetized dog heart in situ. Transmural samples necessary to the repeated determination of tissular substrates were taken from left ventricular wall according to the "drill biopsy" technique: they were made possible by a total cardiopulmonary by-pass system. The beta-adrenergic stimulation was obtained by infusion of isoproterenol (1 microgram/kg/min.) and the ischemia by injection into left coronary artery before its division of a viscous mixture, reducing coronary flow by 40 to 70%. In both subendocardial and subepicardial layers, but mainly in the former: --beta-adrenergic stimulation lowers glycogen content and raises lactate content immediately, lowers free fatty acid concentration more progressively without modifying triglyceride concentration significantly; --ischemia decreases glycogen content and increases lactate content in the same way, but raises free fatty acid and triglyceride concentration. Consequently, beta-adrenergic stimulation and ischemia are likely to add their effects on anaerobic glycolysis, whereas they exert an opposite influence on lipid metabolism.

Adrenergic beta-Agonists↗
PubMedDate not supplied

[Effects of hypocalcemia on atrioventricular conduction compared with those of agents which inhibit the slow channel (author's transl)].

1. The effects of experimental hypocalcemia were studied on 13 anesthetized and atropinized dogs, measuring endocavitary His bundle recordings, global effective refractory period (ERP) (determination by the extrastimulus method), and sinus rate. These data, including arterial pressure, were observed during a 40 min. I.V. infusion of Na EDTA, 3 mg . kg-1 . min-1. We observed: 1.1. A decrease in serum ionized calcium, from 45,7 mg . 1-1 (control) to 28,1 mg . 1-1 1.2. A moderate, though highly significant, decrease in the intraatrial conduction time (SA interval of His bundle recordings). 1.3. A significant increase in the AV node conduction time (AH). 1.4. No significant change in the His-Purkinje system conduction time (HV). 1.5. A significant increase in the global ERP, primarily involving the atrial contractile tissue ERP, and further the atrioventricular node ERP.

Animals↗
PubMedDate not supplied

Influence of the restoration of vagal tone by intracisternal injection of dextromoramide on the cardiac effects of the antiarrhythmic drugs.

The effects of four antiarrhythmic drugs, quinidine, procainamide, amiodarone and verapamil were studied on sinus rate, conduction time and, when possible, effective refractory period (ERP) in atrioventricular node (AV node), and finally atrial muscle ERP. This study was made under two types of conditions, vagal tone being absent or present after restoration in the anesthetized dog by a new technique, the intracisternal injection of dextromoramide. Quinidine and procainamide which tend to slow down sinus rate and conduction in the former case accelerate them considerably in the latter by opposing the effects of acetylcholine released by vagal endings. The prolongation of atrial ERP also induced by these drugs results from both this process and their own capacity. Amiodarone and verapamil, usually responsible for bradycardia, notable delay in AV node conduction and lengthening of AV node ERP are, however, liable to elicit opposite effects, especially amiodarone when vagal tone is very high. The reduction of vagal influence is, in the case of these drugs, the only factor in the prolongation of atrial ERP. In any case, the response of both specialized and common tissue of the heart to antiarrhythmic drugs should not be interpreted unless the degree of vagal tone is known.

Amiodarone↗
PubMedDate not supplied

[Pharmacologic complications of the unequal reactivity of constituent elements of the myocardium to the parasympathetic system].

Pharmacological consequences of the unequal reactivity of the myocardial different parts to parasympathic system. The effects of acetylcholine on the various levels of cardiac automatism are studied on open chest dogs with extracorporeal circulation. This drug depresses the sinus node, and more specially the atrio-ventricular node (AV node), but does not alter the His bundle and the Purkinje fibers activity. The sensitivity of the intra-cardiac conduction to acetylcholine also depends upon the considered level of conduction: measured with a bipolar electrode situated upon the His bundle, this one is lowered electively in the atrio-ventricular part. So, the A, V. node can be considered as the elective place of action of acetylcholine on the double point of view of automatism and conduction. Drugs modifying the vagal tonus see their action altered, either in a plus way (antiarrhythmic agents), either in a minus way (cardiac glycosides, halogenated hydrocarbons).

Acetylcholine↗
PubMedDate not supplied

[Evaluation of the potential cardiotoxicity of propranolol-lithium gluconate association (author's transl)].

The association B blocking agent-lithium salt is used for the therapy of some severe hyperthyroidism with cardiotoxicosis. Separately, both drugs depress intracardiac conduction. However by recording the potentials of the His bundle in anesthetized dogs, a potential cardiotoxicity of this association is unlikely since sinusal automaticity alone is importantly slowed. But, these results need further confirmation in man.

Animals↗
PubMedDate not supplied

[Demonstration of the fibrillatory effect of class I anti-arrhythmia agents based on the time of fibrillation onset and electrical threshold in myocardial ischemia].

In recent clinical studies, certain class I antiarrhythmic drugs (flecaïnide, lidocaïne) appeared to be responsible for an increase in mortality, when used to treat ventricular arrhythmias occurring after or during infarction. Experimentally, in pigs whose rate of ventricular beats was kept constant by pacing, all the studied class I antiarrhythmic drugs, disopyramide, lidocaïne and flecaïnide, proved to be to a variable degree capable of shortening time to onset of fibrillation (TOF) elicited by controlled myocardial ischemia. Fibrillation occurred at the end of the decline, under the influence of ischemia, of electrical fibrillation threshold (EFT) down to near 0 mA. The fall of EFT to this level was checked by ischemias of increasing duration to be hastened by the cited antiarrhythmic drugs. In other words, these drugs exert a profibrillatory effect in the ischemic heart.

Animals↗
PubMedDate not supplied

Vulnerability to ventricular fibrillation related to ischaemia: comparison of the acute effects of beta-blockers and calcium antagonists.

A comparative evaluation of beta-blockers and calcium antagonists as protective agents against ventricular fibrillation related to myocardial ischaemia, was attempted in the pig heart in situ of anaesthetized, open-chest animals, subjected to a temporary complete occlusion of the left anterior descending coronary artery near its origin. This occlusion resulted in fibrillation occurring after a time depending on the vulnerability to the fibrillatory process. As this time to onset of fibrillation does normally not exceed a few minutes, its determination could be achieved repeatedly in the course of an experiment, in the absence and presence of drugs such as beta-blockers and calcium antagonists. When propranolol (0.05 mg/kg, i.v.) and verapamil (0.05 mg/kg, i.v.) abolished tachycardia produced by isoproterenol (0.25 micrograms/kg/min), the triggering of fibrillation was delayed in either case: in animals under atrial pacing at a rate close to the sinus rate on each determination, time to fibrillation was prolonged from about 160 to 400 sec by propranolol and from 160 to 640 sec by verapamil, with a return to control values within 60 min. Under ventricular pacing at a constant high rate (180 beats/min), no change was observed in time to fibrillation after propranolol (0.025 or 0.050 mg/kg), whereas verapamil, in the same conditions and in the same doses, multiplied this time by about 4 and 6, respectively. Consequently, propranolol and verapamil are likely to protect against fibrillation immediately after i.v. injection, but the protection due to propranolol is only indirect and a consequence of bradycardia which tends to increase the polarization of the muscular fibres, whereas verapamil adds to the same influence a direct preventive action by avoiding a cellular calcium overload in these fibres, which is responsible for the depolarization and fluctuations of their membrane potential.

Animals↗
PubMedDate not supplied

[Comparative study of different classes of anti-arrhythmia agents on the vulnerability of ischemic ventricular fibrillation].

A comparative study of the various classes of antiarrhythmic drugs as agents protecting against ischaemia-induced ventricular fibrillation was undertaken in the pig in situ heart, in anaesthetized animals which were subjected to complete temporary occlusion of the left anterior descending coronary artery. This occlusion resulted in fibrillation after a time which varied in inverse ratio to vulnerability to fibrillation. However, as this time did not exceed a few minutes, time to onset of fibrillation could be repeatedly measured in the course of an experiment, in the absence or in the presence of an antiarrhythmic drug. Under ventricular pacing at a constant rate, 180 beats/min, all the class I antiarrhythmic drugs, flecainide, disopyramide and lidocaine, in clinical dose range, reduced time to fibrillation to a large extent (25 to 50%) at the maximum of their action, with gradual return to control values within less than one hour. The enhancement of vulnerability to fibrillation was accompanied by reduction in intraventricular conduction velocity and fibrillation rate. With the same ventricular pacing, no change was observed in time to fibrillation under the influence of propranolol or amiodarone. As for verapamil, it lengthened this time considerably, up to 600%. However, bradycardia produced in usual circumstances ensures a real protection against ischaemic fibrillation with propranolol and amiodarone and enhances protection directly exerted by verapamil.

Animals↗