Protective effect of lidocaine against ischemia and reperfusion-induced arrhythmias and shifts of myocardial sodium, potassium, and calcium content.

Isolated guinea pig hearts subjected to global ischemia, were used to investigate whether lidocaine exerts an antiarrhythmic action against reperfusion-induced arrhythmias, and the effects of this drug upon myocardial ion contents during ischemia and reperfusion were studied. In the first series of experiments, the drug was administered 5 min prior to the induction of global ischemia and maintained during reperfusion. With 3.6 X 10(-6), 7.2 X 10(-6), 14.7 X 10(-6), and 29.5 X 10(-6) mol/L lidocaine, reperfusion-induced ventricular fibrillation and tachycardia were reduced from their control incidence of 83% and 100% to 41% and 58%, 33% (p less than 0.05) and 25% (p less than 0.001), 8% (p less than 0.01) and 8% (p less than 0.001), 0% (p less than 0.001) and 0% (p less than 0.001), respectively. The ion contents of myocardium were determined by atomic absorption spectrophotometer after washout of the ions from vasculature. Ischemia induced a marked accumulation of sodium and loss of potassium in the myocardial tissue. Both ischemia-induced sodium gain and potassium loss were significantly inhibited by lidocaine treatment. During reperfusion, sodium was further increased in the control group and this value was significantly lower in the lidocaine-treated group after 1 min of reperfusion. Sodium content remained at nearly constant level for the rest of reperfusion period. Potassium was suddenly increased during the first 5 min of reperfusion then continuously decreased until the end of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)