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SUMMARY We measured myocardial blood flow and myocardial procainamide concentration in 24 sections of left ventricle following occlusion of the left circumflex coronary artery in 11 dogs. C-Labeled procainamide was infused at a constant rate (40μg/kg Per m +-n) following completion of the coronary artery occlusion. At the end of 4 hours, the infusion was terminated and the dogs were killed. Regional myocardial blood flow was determined at 30 minutes and at 4 hours, usingI2SI- and5>Cr-labeled microspheres. Regional myocardial procainamide concentration was determined by analysis of C content in the samples, using a combustion technique with entrapment of liberated I4CO2. The amount of14C activity in each sample was calculated following corrections made for51Cr andI25I activity, using the channels ratio method. Twenty-four regional sections of left ventricle were divided into 12 anteroseptal control sections and 12 posterolateral ‘ischemic’ sections. Myocardial blood flow to the control region was 1.17 ± 0.17 (mean ± SEM) ml/min per g and myocardial procainamide concentration was 4.62 ± 0.36 μg/g. Plasma procainamide concentration was 2.2 ± 0.1 μg/m+-- Flow to ischemic sections, when measured at 30 minutes and 4 hours, did not change. Myocardial procainamide concentrations in the ischemic sections differed significantly from procainamide in the control sections only when flow fell to 31-40% of control values (P < 0.01). At flows less than or equal to 10% of control flow, myocardial procainamide concentration was reduced to only 42 ± 4% of control drug levels. We conclude that in our experiments there is a substantial concentration of procainamide in severely hypoperfused and probably densely infarcted ventricular myocardium.

Relationship between regional myocardial procainamide concentration and regional myocardial blood flow during ischemia in the dog.