Electrophysiological effects of morphine in an in vitro model of the ‘border zone’ between normal and ischaemic–reperfused guinea-pig myocardium

Abstract

Morphine is commonly used in clinical practice in pain management. Although morphine has been shown to precondition the myocardium, its effects on action potential parameters and ischaemia-reperfusion-induced arrhythmias and conduction blocks remain unknown. In a double-chamber bath, guinea-pig right ventricular muscle strips were subjected partly to normal conditions and partly to 30 min of simulated ischaemia (hypoxia, hyperkalaemia, acidosis, and lack of nutritional substrate) followed by 30 min of reperfusion. Action potential parameters were recorded continuously in the normal zone and in the ischaemic- reperfused zone. Spontaneous arrhythmias and conduction blocks were noted. The electro physiological effects of morphine were studied at 0.01 and 0.1 micro M. In control conditions, morphine did not modify action potential parameters of resting membrane potential, maximal upstroke velocity (V(max)), action potential amplitude (APA) and action potential duration at 50 and 90% of repolarization. Morphine reduced ischaemia-induced depolarization and lessened the ischaemia-induced decrease in APA and V(max). Morphine significantly decreased the occurrence of conduction block during simulated ischaemia (20% at 0.01 and 0.1 micro M vs 67% in the control group, P<0.05) and reperfusion-induced arrhythmias (40% at 0.01 micro M and 30% at 0.1 micro M vs 92% in the control group, P<0.05). In ischaemic-reperfused guinea-pig myocardium, morphine at clinically relevant concentrations decreased ischaemia-induced conduction blocks and reperfusion-induced ventricular arrhythmias.