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C Massé

Publications and source records attributed to C Massé.

6 recordsLinked to original sources
PubMed1990

Bupivacaine-induced slow-inward current inhibition: a voltage clamp study on frog atrial fibres.

The effects of various concentrations of bupivacaine on the characteristics of the slow-inward current (isi) were studied over a ten-minute period on isolated frog atria. At a concentration of 10(-7) M, bupivacaine did not modify isi. At 10(-6) M, the maximal amplitude of the slow-inward current (i max) was depressed by 11 per cent. At 10(-5) M, i max was depressed by 24.5 per cent, the time-to-peak current value (tpeak) was increased by 13.4 per cent and the inactivation time constant (tau in) by 29.8 per cent. At 10(-4) M, i max was depressed by 32.9 per cent, tpeak increased by 30.4 per cent and tau in by 58.7 per cent. In conclusion, bupivacaine produced only moderate inhibition of the slow-inward current. The findings might explain the decline in sinus impulse formation with sinus bradycardia, and the slowing of atrio-ventricular node conduction produced by bupivacaine. However, the decrease in contractility previously reported does not seem to be due only to inhibition of the slow-inward current.

Action Potentials↗
PubMed1989

In vitro study on mechanisms of bupivacaine-induced depression of myocardial contractility.

Although several mechanisms have been proposed to explain bupivacaine cardiotoxicity, the predominant effect remains to be determined. In this study, we used an isolated rabbit right atrial model that reproduces the effects on inotropic and chronotropic functions induced by 0.5 micrograms/mL bupivacaine; then we tried to counteract these events by electrical stimulation or by addition of CaCl2 or adenosine triphosphate (ATP) to the bathing solution. Contractile force was dramatically depressed by bupivacaine alone (-68%), even when the preparation was paced (-59%). CaCl2 partially counteracted this decrease (-37%). Inotropic function was almost completely restored (-9%) when ATP was added before administration of bupivacaine. Inhibition of energy metabolism seems to be a major explanation for bupivacaine cardiotoxicity.

Adenosine Triphosphate↗
PubMed1987

Evidence for a class 4 effect of cibenzoline "in vivo".

In anesthetized dogs, it has already been shown that cibenzoline (4 mg/kg i.v.) possesses class 1 anti-arrhythmic properties. In this work, the cardiac electrophysiologic effects of cibenzoline (1 mg/kg i.v.) were studied before and after propranolol (0.2 mg/kg i.v.) treatment. Cibenzoline caused a slight tachycardia, a reduction of conduction velocity in the His-Purkinje system and in the ventricle, but no significant effects in the atria and the atrioventricular node were detected. On the contrary, when dogs were given the beta-adrenoceptor blocking agent propranolol, cibenzoline produced major effects in the slow response structures, especially in the sinus node and the atrioventricular node (bradycardia and depression of the atrioventricular nodal conduction). No further effects were observed on the His-Purkinje system and ventricle as compared to administration of cibenzoline alone. In dogs, cibenzoline given i.v., had no effects on the slow response systems, probably because of sympathetic nervous system intervention since the class 4 effects of cibenzoline appeared after beta-adrenoceptor blockade.

Anesthesia↗
PubMed1975

Effects of antiarrhythmic drugs on cardiac membrane conductances; a study using the Hodgkin and Huxley mathematical model.

A study in voltage clamp conditions of the modifications of the cardiac membrane conductances by quinidine sulfate has been carried out on frog atrial fibers by means of the double sucrose gap technique. The computation of the parameters related to the conductances has been done according to the Hodgkin and Huxley mathematical model proposed in 1952. The computed conductances concern the sodium conductance, the calcium conductance, and the total delayed conductance. A decrease of all of the studied conductances is observed in the presence of quinidine sulfate. This drug also mainly induced a slowing down of several activation, inactivation, and reactivation kinetics. The results obtained allow a more detailed explanation of the mechanism of action of quinidine sulfate in the membrane. Although quinidine is known to possess antiarrhythmic properties, the exact mechanisms of its action are not clear. The present study was therefore undertaken to provide some information on this point.

Animals↗