Use of cold blood cardioplegia to protect against coronary microcirculatory injury due to ischemia and reperfusion.

The effect of cold blood cardioplegia in preventing microvascular injury owing to myocardial ischemia and reperfusion was studied. Two groups of eight dogs each were placed on cardiopulmonary bypass with separate coronary perfusion at 80 mm Hg. Microcirculatory function was assessed by measuring the extraction and permeability surface area product (PS) for inulin and albumin. These changes were correlated with the transport and extraction of oxygen, coronary blood flow, and morphologic studies of the microvasculature. In Group I, ischemic hearts were kept normothermic for 45 minutes. In Group II, 250 ml of cold (4 degrees C) blood cardioplegic solution (potassium chloride 30 mEq/L) was infused and the infusion repeated at 15 and 30 minutes. Reperfusion resulted in marked reactive hyperemia for Group I (p less than 0.05) but no hyperemic response in Group II. In Group I, but not II, ischemia-reperfusion caused a significant decrease in PS inulin (0.47 +/- 0.10 ml/min/gm) compared to the preischemic value (1.04 +/- 0.23) (p less than 0.05). There was a threefold decrease in the PS inulin/PS albumin ratio with reperfusion in Group I, indicating increased vascular permeability to albumin. There was also a significant decrease in myocardial oxygen consumption (from 5.1 +/- 0.7 to 3.4 +/- 0.5 ml/min/100 gm, p less than 0.05) for Group I. These did not decrease for Group II. Histologic studies showed diffused areas of no reflow in the unprotected hearts. The wet/dry weight ratio for Group I (4.97 +/- 0.09) was significantly greater than for Group II (4.49 +/- 0.07) (p less than 0.001). The results indicate that in the unprotected heart, ischemia-reperfusion caused microcirculatory injury resulting in increased permeability to albumin, edema, a reduction in surface area, and areas of no reflow. In contrast, in the hearts protected with cold blood cardioplegia, no evidence of microcirculatory injury occurred.