Dersham G H, Han J, Cameron J S, O'Connell D P
J Electrocardiol. 1986 Oct;19(4):355-9. doi: 10.1016/s0022-0736(86)81063-9.
The left anterior descending coronary artery was occluded in anesthetized dogs. Dogs were sacrificed after 24 hours and the experimental preparations, which included both normal and infarcted tissues, were dissected from the left ventricles. Effects of tocainide in concentrations of 15-40 mg/l on action potentials of Purkinje fibers from normal and infarcted zones were studied using conventional microelectrode techniques. In the normal zone cells, tocainide superfusion produced a significant decrease in maximum diastolic potential, action potential amplitude, action potential duration to 50% and 90% repolarization and the rate of phase O depolarization, and no significant change in effective and functional refractory periods. In the infarct zone cells, it produced a significant decrease in action potential amplitude and the rate of phase O depolarization, a significant increase in effective and functional refractory periods, and no significant changes in the other parameters. The unequal actions of tocainide resulted in selective depression of maximum diastolic potential and action potential duration to 50% repolarization in the normal cells only, reducing the disparity in these parameters between normal and infarcted tissues. Tocainide increased the refractoriness (ratio of effective refractory period to action potential duration) in both cell types but this change was greater in the infarct zone. This decreased disparity of membrane potential and repolarization combined with increased refractoriness may help to block the arrhythmias observed in infarcted preparations following closely coupled stimuli.