Cardiopulmonary bypass during reperfusion after coronary occlusion attenuates the "no reflow" phenomenon in ischemic myocardium.

There is increasing interest in providing reperfusion after coronary occlusion to preserve myocardium and to decrease infarct size. This study was conducted to assess the protective effect of normothermic coronary bypass on myocardial salvage during reperfusion, to evaluate the redistribution of regional myocardial blood flow (RMBF), and to study the extent of the “no reflow” phenomenon. Twelve dogs were subjected to 3 hours of left anterior descending (LAD) occlusion. After release of the occlusion, Group I had 3 hours' reperfusion without cardiopulmonary bypass (CPB) and Group II had 90 minutes' reperfusion with CPB followed by 90 minutes' reperfusion without CPB. The area at risk was determined by monastryl blue injection into the left atrium; the area of necrosis was determined planimetrically from left ventricular areas unstained by triphenyltetrazolium chloride (TCC). The endocardial/epicardial blood flow (ml/min/100 gm LV) of the central ischemic area was determined before LAD occlusion, 20 minutes after reperfusion, and 170 minutes after reperfusion with 8 to 10 μ radionuclide-labeled microspheres. The mean area at risk, expressed as a percent of the left ventricle, and the mean area of necrosis, expressed as a percent of the area at risk, did not differ significantly in either group (Group I, 68.7%; Group II, 62.1%). The RMBF before coronary occlusion and 20 and 170 minutes after release of the LAD occlusion showed that the control zones for LAD occlusion were similar in both groups of dogs that the endocardial/epicardial ratio in the central ischemic zone was significantly higher in Group II (CPB) than in Group I (no CPB). In Group I the endocardial/epicardial ratio was 48/131 ml/min/100 gm LV at 20 minutes and decreased to 11.9/96.4 at 170 minutes. In Group II, after CPB, this ratio went from 47.4/90.8 ml/min/100 gm LV at 20 minutes to 35.4/95.9 at 170 minutes. The difference in the endocardial/epicardial ratios in the central ischemic zone between the two groups at 20 and 170 minutes was significant to the 0.001 level. Thus CPB during reperfusion does not increase myocardial injury. In fact, the reduction of endocardial blood flow in the central ischemic zone, progressive during reperfusion in the working heart, is attenuated following reperfusion in the beating, nonworking heart on CPB.