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European Heart Journal 1994 15(3):418-423;
Copyright © 1994 by the European Society of Cardiology.
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© 1994 The European Society of Cardiology

Early accumulation of the terminal complement-complex in the ischaemic myocardium after reperfusion

D. MATHEY*,, J. SCHOFER*,, H. J. SCHÄFER{dagger}, T. HAMDOCH*, H. C. JOACHIM*, A. RITGEN*, F. HUGO{ddagger} and S. BHAKDI§

*Department of Cardiology, University Hospital Eppendorf Hamburg, Germany
{dagger}Department of Pathology, University Hospital Eppendorf Hamburg, Germany
{ddagger}Institutes of Medical Microbiology, Universities of Gießen Germany
§Institutes of Medical Microbiology, Universities of Mainz Germany

Received 16 December 1992; revised 19 October 1993; .

Correspondence Prof Dr D. Mathey/Prof. Dr J. Schofer und Partner, Innere Medizin-Kardiologie, Othmarscher Kirchenweg 168, 22763 Hamburg, Germany

Abstract

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.

Key Words: Complement system • myocardial infarction • reperfusion injury


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