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

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. ¹⁴C-labeled procainamide was infused at a constant rate (40 μg/kg per min) 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, using ¹²⁵I- and ⁵¹Cr-labeled microspheres. Regional myocardial procainamide concentration was determined by analysis of ¹⁴C content in the samples, using a combustion technique with entrapment of liberated ¹⁴CO₂. The amount of ¹⁴C activity in each sample was calculated following corrections made for ⁵¹Cr and ¹²⁵I 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/ml. 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.