Effects of intracoronary potassium chloride on electrograms of canine Purkinje fibers in six-hour- to four-week-old myocardial infarcts. An indication of time-dependent changes in collateral blood flow.

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Abstract
Canine hearts were isolated 6 h, 24 h, 3 days, 6 days and 4 wk after coronary artery ligation and were perfused with blood from support dogs. Electrograms were recorded from Purkinje fibers in the infarcted zone and from Purkinje fibers and ventricular muscle in noninfarcted areas. Administration of 2.5 meq of KCl into the coronary circulation of the infarcted hearts abolished noninfarcted zone electrograms within 2-8 s, indicating rapid delivery of a high concentration of K+ to areas receiving normal coronary blood flow. Intracoronary KCl had no effect on the infarct zone Purkinje fiber electrograms recorded from hearts with 6 h infarcts, indicating very low or absent coronary flow. In 24 h infarcted hearts, intracoronary KCl depressed the amplitude of most infarct zone Purkinje fiber electrograms but did not abolish them, suggesting some return of capillary flow. Most infarct zone Purkinje electrograms in older (3 day to 4 wk) infarcts were rapidly abolished after intracoronary KCl, suggesting that capillary flow returned to normal. Very low or absent blood flow to subendocardial Purkinje fibers 6 h after infarction may cause the abnormalities in their transmembrane potentials and the return of blood flow may cause infarct zone Purkinje fiber transmembrane action potentials to return to normal. KCl administered into the left ventricular cavity abolished electrical activity in the subendocardial Purkinje fibers but did not alter the ectopic ventricular rate or rhythm of hearts with 6 h infarcts and abolished the ventricular arrhythmia in only 1 of the 3 hearts with 24 h infarcts, indicating that some of the delayed ventricular arrhythmias after coronary occlusion arise from sites other than the subendocardial Purkinje system.