Atsuumi T, Yaoita H, Shichishima T, Maehara K, Fujita T, Maruyama Y
First Department of Internal Medicine, Fukushima Medical University, Japan.
Jpn Circ J. 2001 Jul;65(7):659-66. doi: 10.1253/jcj.65.659.
Cobra venom factor (CVF) transiently activates polymorphonuclear leukocytes (PMN) by complement activation, followed by rapid complement depletion and gradual reversal of PMN activation. Utilizing these sequential changes caused by CVF, the individual and combined effects of complement and PMNs on myocardial infarct size (IS) were investigated. Rats were treated with CVF, and/or anti-PMNs. Complement was depleted, but circulating PMNs were being activated at 4h after CVF administration, and at 36h after, complement was depleted, but PMNs were in a near basal condition. Under anesthesia, the rats had a 30-min coronary occlusion followed by 6h of reperfusion. The IS was assessed by tetrazolium staining. CVF, as well as anti-PMNs, reduced myeloperoxidase (MPO) activity in the risk area and the reduced MPO resulted in a reduced IS, which was also the effect of anti-PMNs, but complement depletion by CVF, during which circulating PMNs were activated, failed to reduce the IS despite low MPO activity. These results suggest that complement and the condition of PMNs each play a role in determining the IS, and ischemic reperfusion injury might be produced even by relatively low myocardial MPO activity.
眼镜蛇毒因子（CVF）通过补体激活短暂激活多形核白细胞（PMN），随后补体迅速耗竭，PMN激活逐渐逆转。利用CVF引起的这些顺序变化，研究了补体和PMN对心肌梗死面积（IS）的单独和联合作用。用CVF和/或抗PMN处理大鼠。补体耗竭，但在给予CVF后4小时循环中的PMN被激活，在36小时后，补体耗竭，但PMN处于接近基础状态。在麻醉下，大鼠冠状动脉闭塞30分钟，随后再灌注6小时。通过四氮唑染色评估IS。CVF以及抗PMN降低了危险区域的髓过氧化物酶（MPO）活性，MPO降低导致IS减小，这也是抗PMN的作用，但在循环中的PMN被激活期间，CVF导致的补体耗竭尽管MPO活性较低，但未能减小IS。这些结果表明，补体和PMN的状态在决定IS方面均起作用，并且即使心肌MPO活性相对较低也可能产生缺血再灌注损伤。
