Contractile reserve and left ventricular function in regional myocardial ischemia in the dog.

Contractile activity remaining in a region made ischemic by acute occlusion of the left anterior descending coronary artery (LAD) was assessed in dogs relative to its role in maintaining left ventricular (LV) function. Compensatory increases in contractility of normal myocardium were eliminated by treating all dogs with reserpine (3 mg/kg) to deplete their catecholamine stores. LV function was determined by measuring stroke volume while increasing the LV filling pressure with a shunt from the aorta to left atrium. Heart rate and mean aortic pressure were kept constant. LV function was studied after occlusion of the LAD alone and after the selective infusion of potassium chloride (1 mEq/ml) into the LAD to raise the regional extracellular potassium concentration to 30 mEq/ml. The reduction in LV function induced by LAD ligation was less than the reduction caused by abolishing contraction in the entire zone supplied by the LAD with infusion of potassium. The totally cardioplegic zone induced by potassium amounted to 20.3-39.8% of the LV mass. At an LV end-diastolic pressure of 12 mm Hg, stroke volume (SV) was reduced in proportion to the size of the cardioplegic zone: -SV (% volume) = -1.55% (% of LV mass) + 120.1 (r = -0.69, p less than 0.005). Thus, a dyskinetic zone of 35% of the left ventricle reduced stroke volume by 34% when adrenergic compensation was blocked. We conclude that residual transmural contractility exists in the ischemic region of myocardium subserved by an obstructed LAD and contributes significantly to LV function.