McDonagh P F, Laks H
J Thorac Cardiovasc Surg. 1982 Oct;84(4):609-18.
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.
研究了冷血心脏停搏液在预防心肌缺血再灌注所致微血管损伤中的作用。将两组各8只犬置于体外循环，冠状动脉以80 mmHg的压力单独灌注。通过测量菊粉和白蛋白的摄取及通透面积乘积（PS）来评估微循环功能。这些变化与氧的转运和摄取、冠状动脉血流量以及微血管的形态学研究相关。在第一组中，缺血心脏保持常温45分钟。在第二组中，输注250 ml冷（4℃）血心脏停搏液（氯化钾30 mEq/L），并在15分钟和30分钟时重复输注。再灌注导致第一组出现明显的反应性充血（p＜0.05），而第二组无充血反应。与缺血前值（1.04±0.23）相比，第一组但非第二组的缺血再灌注导致菊粉PS显著降低（0.47±0.10 ml/min/gm）（p＜0.05）。第一组再灌注时菊粉PS/白蛋白PS比值降低了三倍，表明血管对白蛋白的通透性增加。第一组心肌耗氧量也显著降低（从5.1±0.7降至3.4±0.5 ml/min/100 gm，p＜0.05）。第二组则未降低。组织学研究显示未保护心脏中有弥漫性无复流区域。第一组的湿/干重比值（4.97±0.09）显著高于第二组（4.49±0.07）（p＜0.001）。结果表明，在未保护的心脏中，缺血再灌注导致微血管损伤，从而使白蛋白通透性增加、水肿、表面积减少以及出现无复流区域。相比之下，在用冷血心脏停搏液保护的心脏中，未出现微血管损伤的证据。
