Sublytic complement attack reduces infarct size in rabbit isolated hearts: evidence for C5a-mediated cardioprotection

Immunopharmacology Pub Date : 2000-09-01 Epub Date: 2000-09-14 DOI:10.1016/S0162-3109(00)00258-7
Elaine J Tanhehco, Heekyung Lee, Benedict R Lucchesi
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引用次数: 13

Abstract

Sublytic complement attack can elicit protective cellular responses without precipitating cell death. Our investigation examined the effects of non-lethal complement activation in isolated hearts. New Zealand white rabbit hearts were subjected to 30 min of ischemia followed by 1 h of reperfusion. Prior to ischemia, hearts were perfused for 20 min with 0.5% normal human plasma (NHP). Hearts treated with NHP developed significantly (p<0.05) smaller infarcts compared with controls, expressed as percent of area at risk (AAR) (25.3±4.0% vs. 40.9±4.3%, respectively). Heat-inactivation, soluble complement receptor 1 (sCR1; 20 nM), and anti-C5a antibody reversed the protective effect of NHP (39.0±3.1%, 41.7±5.1% and 38.4±2.3% AAR, respectively). Hearts treated with 3 nM C5a exhibited infarct sizes similar to those exposed to NHP (27.6±5.0% AAR). sCR1 alone did not affect infarct size (37.9±4.5% AAR). The results suggest that non-lethal complement activation attenuates reperfusion injury through formation of C5a.

溶解体攻击减少兔离体心脏梗死面积:c5a介导的心脏保护证据
亚溶解体攻击可引起保护性细胞反应而不引起细胞死亡。我们的研究考察了非致死性补体激活对离体心脏的影响。新西兰大白兔心脏缺血30 min,再灌注1 h。缺血前,用0.5%正常人血浆(NHP)灌注心脏20分钟。与对照组相比,使用NHP治疗的心脏梗死面积明显缩小(p<0.05),以危险面积百分比(AAR)表示(分别为25.3±4.0%和40.9±4.3%)。热失活可溶性补体受体1 (sCR1);抗c5a抗体逆转了NHP的保护作用(分别为39.0±3.1%、41.7±5.1%和38.4±2.3%)。3 nM C5a处理的心脏梗死面积与NHP处理的心肌梗死面积相似(27.6±5.0% AAR)。单独sCR1不影响梗死面积(37.9±4.5% AAR)。结果表明,非致死性补体激活通过C5a的形成减轻再灌注损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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