ABSTRACT
The effect of varying the extent of regional ischemia on in situ end-systolic pressurevolume relationships (ESPVRs) was examined in six open-chest canine left ventricles. Randomly selected proximal or distal sites of either circumflex or left anterior descending (LAD) arteries were occluded for 3 min. Left ventricular pressure-volume data were obtained using the conductance (volume) catheter technique, with loading altered by transient inferior vena caval occlusion. Radiolabeled microspheres were used to determine regional myocardial blood flow, and the total extent of ischemia was defined by the percent of left ventricular mass with ≤50% baseline flow. Animals were studied after autonomic blockade induced by hexamethonium and vagotomy. The slope of the ESPVR or end-systolic elastance (Ees) was reduced from baseline in nearly every occlusion. This reduction in Ees significantly correlated with the extent of ischemic injury (%I) – (%ΔEes = −1.4 · %I + 2.1, p <0.005). The ESPVRs were shifted rightward, with an increase in end-systolic volume (Ves) at a common end-systolic pressure which also correlated to the extent of ischemia (ΔVes = 0.59 · %I − 1.2, p<0.005). The two-compartment model of regional ischemia is reexamined, and the influences of baseline Ees, diastolic chamber stiffness, ambient end-systolic pressures, and potential remote-ischemic region interactions are explored to explain differences between the in situ data and previous data from isolated, isovolumically contracting canine ventricles.
