EARLY ACCUMULATION OF THE TERMINAL COMPLEMENT-COMPLEX IN THE ISCHEMIC MYOCARDIUM AFTER REPERFUSION

被引:75
作者
MATHEY, D
SCHOFER, J
SCHAFER, HJ
HAMDOCH, T
JOACHIM, HC
RITGEN, A
HUGO, F
BHAKDI, S
机构
[1] UNIV HOSP EPPENDORF,DEPT CARDIOL,HAMBURG,GERMANY
[2] UNIV HOSP EPPENDORF,DEPT PATHOL,HAMBURG,GERMANY
[3] UNIV MAINZ,INST MED MICROBIOL,W-6500 MAINZ,GERMANY
[4] UNIV GIESSEN,INST MED MICROBIOL,W-6300 GIESSEN,GERMANY
关键词
COMPLEMENT SYSTEM; MYOCARDIAL INFARCTION; REPERFUSION INJURY;
D O I
10.1093/oxfordjournals.eurheartj.a060516
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The terminal membrane-damaging complement complex C5b-9 accumulates in the infarcted myocardium. In experimental myocardial infarction, we investigated the time course of C5b-9 deposition and the influence of reperfusion. In a group of 17 rabbits (group 1), the circumflex coronary artery was occluded for different time periods ranging from 0.5 to 29 h without subsequent reperfusion. A second group of 23 rabbits (group 2) underwent coronary artery occlusion for periods ranging from 0.5 to 6 h followed by reperfusion. C5b-9 was determined in transmural myocardial biopsies by immunohistochemistry and by ELISA. In group 1, C5b-9 accumulation in the ischaemic myocardium was found only after 5 to 6 h of coronary artery occlusion. In group 2 (ischaemia and reperfusion), significant C5b-9 deposition was already observed after 30 min of myocardial ischaemia. We conclude that in the absence of reperfusion C5b-9 accumulation occurs as a late event when most of the jeopardized myocardium has probably already become necrotic. In the presence of reperfusion, however, the complement system is activated rapidly and this could play a role in the pathogenesis of reperfusion injury.
引用
收藏
页码:418 / 423
页数:6
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