Reciprocal functional interaction of adjacent myocardial segments during regional ischemia: an intraventricular loading phenomenon affecting apparent regional contractile function in the intact heart.

The mechanism of the increase in function in myocardial segments adjacent to those subjected to regional ischemia is not known. To investigate the hypothesis that changes in regional loading are an important causative factor of this phenomenon, 17 dogs were instrumented with segmental shortening sonomicrometers in the left anterior descending and circumflex artery distributions, circumflex coronary flow probes and cuff occluders, as well as circumflex coronary pressure catheters. Additionally, the animals had aortic pressure catheters and ventricular pressure micromanometers. This animal model allowed modulation of regional inotropic state with regional ischemia or isoproterenol administration. With circumflex coronary bed ischemia, segmental shortening in the circumflex distribution decreased from 11.9 to 6.3% (p = 0.001) whereas left anterior descending regional shortening increased from 11.6 to 13.4% (p less than 0.001). These reciprocal changes occurred in the absence of changes in global afterload or heart rate. Systemic beta-receptor blockade did not change this response, suggesting that it was not reflex- or catecholamine-mediated. Infusing isoproterenol into the circumflex coronary artery resulted in an increase in circumflex regional shortening from 12.5 to 17.4% (p less than 0.02) whereas left anterior descending regional shortening decreased from 13.5 to 8.3% (p less than 0.001), again without change in heart rate or left ventricular or aortic pressure. These data suggest that reciprocal functional interaction between adjacent myocardial segments is a result of changes in regional afterload for the most part, with changes in local preload and timing of ejection also contributing to the observed effect.