Hyperkinetic contraction of a nonischemic segment of ischemic left ventricle in anesthetized dogs

Summary

Regional myocardial function during acute coronary artery occlusion was studied with ultrasonic dimension gauges in 20 open-chest anesthetized dogs. Two pairs of ultrasonic crystals were implanted in the left ventricular free wall near the epicardium in an ischemic segment and in a control nonischemic segment, and the segment length (SL) and maximum velocity of systolic shortening (max dL/dt) were measured. In six dogs, the wall thickness (WT) was measured simultaneously in the same regions with sonomicrometry. Left ventricular pressure (LVP), aortic pressure (AoP), and plasma norepinephrine concentration in the coronary sinus (NE_CS) were also measured. The heart rate was kept constant (180 beats/min) with atrial pacing. The left anterior descending coronary artery was occluded at its distal portion without propranolol in 12 dogs (group 1) and 30 min after propranolol in eight dogs (group 2). In the ischemic region, coronary artery occlusion resulted in an increase in end-diastolic SL (50% at 3 min after occlusion in group 1,P<0.005), and a decrease in max dL/dt in systole (36% at 5 min after occlusion in group 1,P<0.02). In the nonischemic region, end-diastolic SL did not change significantly, but an increase in max dL/dt (29% at 10 min after occlusion in group 1,P<0.005) was observed in systole. Under propranolol (group 2), the results were similar to those of group 1. There were no significant changes in LVP, AoP, and NE_CS during occlusion. We conclude that: (1) SL and WT in the same region present a mirror image, suggesting that WT is a useful index for evaluating regional myocardial function; (2) after coronary artery occlusion, while the ischemic region showed hypokinesis, the nonischemic region presented significant hyperkinesis without an increase in preload (end-diastolic SL) or a decrease in ventricular afterload (AoP); and (3) since these results did not change significantly after propranolol and were not accompanied by an increase in NE_CS, the hyperkinesis in the nonischemic region does not seem to be related toβ-adrenergic receptors and is not due to the Frank-Starling mechanism.