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Summary: 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 l0−6x14.7 x 10−6 and 29.5 x 10−6mol/L lidocaine. reperfusion-induced ventricular fibrillation and tachycardia were reduced from their control incidence of 83% and 100% to 41% and 58%. 33% (p < 0.05) and 25% (p < 0.001). 8% (p < 0.01) and 8% (p < 0.001). 0% (p < 0.001) and 0% (p < 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 I 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. Lidocaine (14.7 x 10 6 mol/L) significantly reduced the sudden increase of potassium in the first few minutes of reperfusion as well as its decline in the further course of reperfusion. Ischemia induced a moderate accumulation of tissue calcium only followed by a steep increase in calcium from the seventh minute of reperfusion. These changes were not influenced by lidocaine. The results obtained describe time-dependent changes of myocardial ion contents in the course of ischemia and reperfusion. and indicate that the protective effect of lidocaine against ischemia-, and reperfusion-induced arrhythmias may be due to the effect of this drug preventing ion movements induced by the above pathologic changes.
Tósaki et al. (Thu,) studied this question.