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. "C-Labeled procainamide was infused at a constant rate (40 jig/kg P r 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, using Iand 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 CO2. The amount of C activity in each sample was calculated following corrections made for Cr and I 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 /ig/g. Plasma procainamide concentration was 2.2 ± 0.1 Mg/'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.