Tetsuji Kaminishi

Effect of diltiazem on coronary blood flow distribution in dog heart under ischemia

Effect of intracoronary infusion of diltiazem (1 μg/min) on regional myocardial blood flow (RMBF) was studied using 15-μm radioactive microspheres in 11 excised cross-circulated canine left ventricles. With total coronary blood flow (CBF) and heart rate (HR) held constant, regional ischemia was induced by ligating the left anterior descending coronary artery (LAD). Diltiazem at the dose used had no effects on ventricular Emax before and after LAD ligation. RMBF expressed by the counts divided by the counts averaged in ail segments in each layer significantly (p < 0.05) increased under diltiazem only in the low-flow region that had <50% RMBF before diltiazem; from 21% (±12%) to 35% (± 18%) in the epicardial, from 22% (± 12%) to 32% (±18%) in the midwall, and from 24% (±10%) to 31% (±12%) in the endocardial layers. We conclude that the beneficial effect of diltiazem on the ischemie heart involves a direct action on the coronary vascular system and does not necessarily depend on the concomitant changes in hemodynamics.

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

SummaryRegional 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 (NECS) 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 NECS 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 NECS, the hyperkinesis in the nonischemic region does not seem to be related toβ-adrenergic receptors and is not due to the Frank-Starling mechanism.