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下肢缺血后再灌注可导致局部损伤(如肌肉水肿和坏死)和远处损伤(如肺微血管通透性增加和中性白细胞逸出)。由于在严重下肢缺血及呼吸衰竭病人中有全身性C_(3a)和C_(5a)水平的升高,有假说在这类病中存在着补体激活。为评价阻断补体激活对防止下肢缺血-再灌注后局部及远处损伤的作用,用S-D雄鼠(450～550克)作实验。在鼠后肢大转子以上用止血带束扎4小时造成下肢缺血。3小时55分时,静脉注入2μCi~(125)Ⅰ标记的牛血白蛋白(BSA),解除束扎,再灌注期为每小时静脉注入0.9％生理盐水1.5ml,总量6.7ml。去除止血带前,静脉注射含可溶性人补体受体1型(sCR1)的磷酸盐缓冲盐水,含量分别为每只鼠1、3、6mg,
Reperfusion after lower limb ischemia can lead to local injuries such as muscle edema and necrosis and distant injuries such as increased pulmonary microvascular permeability and neutrophil leakage. Due to elevated levels of systemic C_ (3a) and C_ (5a) in patients with severe lower extremity ischemia and respiratory failure, there is a hypothesis that there is complement activation in these diseases. To evaluate the effect of blocking complement activation on the prevention of local and distant injury following ischemia-reperfusion of the lower extremities, S-D male rats (450-550 g) were used for the experiment. Hind limbs in the greater trochanter with a tourniquet for 4 hours strangulation caused by lower limb ischemia. Three hours and 55 minutes, 2μCi ~ (125) Ⅰ labeled bovine serum albumin (BSA) was intravenously injected and ligated. The reperfusion period was 1.5ml of 0.9% saline intravenously per hour, with a total volume of 6.7ml. Prior to removal of the tourniquet, phosphate buffered saline (PBS) containing soluble human complement receptor type 1 (sCR1) was intravenously injected at 1,3,6 mg /