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

SUMMARY

Canine hearts were isolated 6 hours, 24 hours, 3 days, 6 days, and 4 weeks 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 KC1 into the coronary circulation of the infarcted hearts abolished noninfarcted zone electrograms within 2-8 seconds, indicating rapid delivery of a high concentration of K+ to areas receiving normal coronary blood flow. Intracoronary KC1 had little or no effect on the infarct zone Purkinje fiber electrograms recorded from hearts with 6-hour infarcts, indicating very low or absent coronary flow. In 24-hour infarcted hearts, intracoronary KC1 depressed the amplitude of most infarct zone Purkinje fiber electrograms but did not abolish them, suggesting some return of capillary flow by this time. Most infarct zone Purkinje electrograms in older (3-day to 4-week) infarcts were rapidly abolished after intracoronary KC1, suggesting that capillary flow returned to normal. Thus, the very low or absent blood flow to subendocardial Purkinje fibers 6 hours after infarction may cause the abnormalities in their transmembrane potentials which have previously been reported, and the return of blood flow with time may be responsible for the return of infarct zone Purkinje fiber transmembrane action potentials to normal. In addition, KC1 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-hour infarcts, and abolished the ventricular arrhythmia in only one of the three hearts with 24-hour infarcts, indicating that some of the delayed ventricular arrhythmias after coronary occlusion arise from sites other than the subendocardial Purkinje system. cire Res 44: 392-405, 1979

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