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Biomedical subjects

M Lakhal

Publications and source records attributed to M Lakhal.

26 records · Page 2Linked to original sources
PubMedDate not supplied

Frequency- and time-dependent depression of ventricular distal conduction by two novel antiarrhythmic drugs, cibenzoline and flecainide.

The effects of two novel antiarrhythmic drugs, cibenzoline and flecainide, known to exert potent inhibitory effects on sodium channel, were investigated on intraventricular conduction in anaesthetized, closed-chest dogs. During this study, in which the heart was electrically stimulated, the pacing period was gradually reduced in the 500-200 msec range, and the pacing rate was abruptly altered (2 sec) or sustained (8 to 10 sec) in order to study the possible frequency- and time-dependency of the depression of conduction. In addition to the electrocardiogram, the conduction time was recorded in the ventricular contractile tissue between an electrode advanced to the apex and the pacing electrode positioned near the base. Effective refractory period (ERP) was concurrently measured according to the extrastimulus method, and the monophasic action potential (MAP) recorded. The drugs were infused at a rate of 0.2 mg/kg/min over a 10 min period after a 4.0 mg/kg loading dose. Conduction time was lengthened by approximately 50% at low frequencies and 100% at high frequencies. Widening of the ORS complexes paralleled this lengthening, whereas the drugs tended only to prolong ERP, without preventing its shortening induced by acceleration. Cardiac disorders were aggravated when high pacing rates were maintained for 8 to 10 sec.

Action Potentials↗
PubMedDate not supplied

Vagal role in potentiation by Ca2+ ions of the action of cardiac glycosides on the atrial specialised tissue.

The combined effects of digoxin and hypercalcaemia were studied in the canine heart in situ on the sinoatrial (SA) and atrioventricular (AV) nodes. Measurements were made of heart rate, of conduction time in the AV node by the endocavitory recording of the His bundle potentials, and of the effective refractory period of this node by the extrastimulus method. In the presence of acetylcholine released by vagal endings or infused into the coronary blood, an increase in plasma calcium concentration from 2.50 to 4.60 mmol/l after a 80 micrograms/kg dose of digoxin considerably depressed conduction in the AV node and automatism in the SA node. In the absence of acetylcholine, no bradycardia occurred under the influence of digoxin alone or digoxin and hypercalcaemia, and hypercalcemia enhanced to a lesser extent digoxin-induced depression of conduction in the AV node. These results evidence a potentiation by acetylcholine of the combined effects of digoxin and hypercalcaemia on the SA and AV nodes.

Acetylcholine↗