Regional function, blood flow, and oxygen utilization relations in repetitively occluded-reperfused canine myocardium.

Temporary coronary occlusion followed by reperfusion severely reduces contractile function in the involved segment. We tested whether an uncoupling exists between O2 utilization (MVO2) and systolic shortening in the ischemic-reperfused segment subjected to repetitive coronary occlusion and reperfusion. In 10 anesthetized open-chest dogs, left ventricular pressure and segment length (sonomicrometry) relations were measured in the left anterior descending (LAD, ischemic-reperfused) segment and circumflex coronary artery (nonischemic segment). Four 12-min LAD occlusions were each followed by 30 min reperfusion. MVO2 was determined in both segments by transmural blood flow (15 microns microspheres) and regional coronary arterial-venous O2 extraction after each occlusion-reperfusion period. The four occlusion-reperfusion periods did not produce necrosis by staining with triphenyltetrazolium chloride. LAD occlusion produced dyskinesis [control = 16 +/- 3.0% systolic shortening (SS) vs. -8.8 +/- 1.5%, P less than 0.0001]. The first reperfusion restored SS only to 2.3 +/- 2.0%, which progressively deteriorated to -3.9 +/- 1.1% (P less than 0.05) with subsequent occlusion-reperfusion episodes. Relative to the nonischemic segment, MVO2 in the ischemic-reperfused segment decreased by only 18% despite dyskinesis. Pressure-length analysis showed systolic stiffening during reperfusion with displacement of the passive ischemic pressure-length loop to the left. Segment work (integral of each loop) continued to be generated at 34.5% of control levels after the last occlusion-reperfusion event in contrast to the negative SS. We conclude that 1) MVO2 in the ischemic-reperfused segment without necrosis remains elevated despite severe reductions in systolic shortening, and 2) the discrepancy between systolic shortening and MVO2 is partially due to persistent development of segment work.