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[急性心肌梗死的发病机制。I. 体内补体激活与梗死的发展]

[Pathogenesis of acute myocardial infarction. I. Complement activation in vivo and development of infarction].

作者信息

Reyes P A, Fernández de la Reguera G, Enríquez C

出版信息

Arch Inst Cardiol Mex. 1984 Jul-Aug;54(4):327-32.

PMID:6497495
Abstract

We studied 53 patients within 12 hs from the onset of symptoms of acute myocardial infarction, and 25 healthy controls. We searched for complement split products in plasma treated with EDTA to avoid in vitro complement activation. Therefore the presence of proteolytic degradation products of C3 signals in vivo activation. Sixteen of the 53 cases (30%), had C3 splitting products in EDTA-plasma. In contrast only 2 (8%) controls showed C3 splitting products. In vivo complement activation correlated with the severity of the infarction.

摘要

我们研究了53例急性心肌梗死症状发作后12小时内的患者以及25名健康对照者。我们在经乙二胺四乙酸(EDTA)处理的血浆中寻找补体裂解产物,以避免体外补体激活。因此,C3信号的蛋白水解降解产物的存在表明体内有激活现象。53例患者中有16例(30%)在EDTA血浆中有C3裂解产物。相比之下,只有2名对照者(8%)显示有C3裂解产物。体内补体激活与梗死严重程度相关。

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