| Autor: |
Duriez PR, Adamantidis MM, Aniq-Filali O, Rouet RH, Dupuis BA |
| Jazyk: |
francouzština |
| Zdroj: |
Journal de pharmacologie [J Pharmacol] 1985 Jan-Mar; Vol. 16 (1), pp. 75-90. |
| Abstrakt: |
Ventricular strips of guinea-pig left myocardium were placed in a special tissue bath bisected by a thin membrane latex. One of the two compartments was flowed during 2 hours with modified Tyrode's solution in order to mimic the in vivo ischemia-induced effects. Replacement in standard conditions during 30 minutes was considered as representative of ischemic heart reperfusion. The second compartment was maintained in standard conditions throughout the experimental time course. Cellular electrical activity was recorded using standard microelectrode technique. Enzyme leakage was appreciated by creatine-kinase (CK) dosage in the effluent from each compartment. Ischemia induced well-known alterations in transmembrane action potentials and led fast-depressed action potentials and decremential responses to appear. Inexcitability occurred within 32 +/- 7 min of ischemia. CK leakage reached 80 +/- 10 I.U. per gram of myocardium dry weight (I.U./g dry) in ischemic chamber and 14 +/- 4 I.U./g dry in normal chamber. Three concentrations (1.10(-8) M, 1.10(-7) M, 1.10(-6) M) of nicardipine were studied. The two highest concentrations significantly decreased CK leakage and totally abolished decremential responses but did not modify the period while each stimulus elicited an action potential. During reperfusion, nicardipine did not significantly modify CK leakage but concentrations of 1.10(-7) M and 1.10(-6) M restored excitability in all preparations (versus 10 p. cent in control ischemia). Action potential characteristics but duration which remained inhomogeneously shortened, returned to almost normal values. The CK leakage decrease during ischemia and the recovery of excitability during reperfusion support a cardioprotective effect of nicardipine. A delay in ischemia-induced calcium overload via the voltage-operating channel is suggested as a possible mechanism for the beneficial effect of slow channel inhibitors. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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