Circulation, Vol 66, 121-128, Copyright © 1982 by American Heart Association
C Yoran, EH Sonnenblick and ES Kirk
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.
ARTICLES
Contractile reserve and left ventricular function in regional myocardial ischemia in the dog