Horstick Georg
2nd Medical Clinic, Johannes Gutenberg-University Mainz, Germany.
Immunobiology. 2002 Sep;205(4-5):552-62. doi: 10.1078/0171-2985-00154.
Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events including complement activation play important roles. Cardioprotection by complement inhibition inter alia C1-esterase-inhibitor (C1-INH) was examined in several experimental models and under clinical conditions with ischemia and reperfusion. C1-INH reduced local anaphylatoxin release revealing the importance of the classical complement pathway. Inhibition of local complement activation was accompanied by improvement of myocardial function and perfusion of the previously ischemic myocardium. Leukocyte endothelial cell-cell interaction was strikingly reduced in the reperfused tissues as afflection of anti-inflammatory effect.
缺血引起的心肌损伤可因梗死区域的再灌注而加重。确切的潜在机制尚未明确，但包括补体激活在内的促炎事件起重要作用。在多种实验模型以及缺血再灌注的临床情况下，研究了补体抑制尤其是C1酯酶抑制剂（C1-INH）的心脏保护作用。C1-INH减少了局部过敏毒素的释放，揭示了经典补体途径的重要性。局部补体激活的抑制伴随着心肌功能的改善以及先前缺血心肌灌注的改善。作为抗炎作用的体现，再灌注组织中白细胞与内皮细胞间的相互作用显著减少。
