Time course of complement activation and inhibitor expression after ischemic injury of rat myocardium.
作者： S Meri , P Laurila , B P Morgan , I Tikkanen , K Helin
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摘要: Activation of the complement (C) system has been documented in both experimental and clinical studies myocardial infarction, but exact time course mechanisms leading to C activation have remained unclear. Our earlier postmortem study on human beings showed that formation membrane attack complex (MAC) was associated with loss CD59 (protectin), an important sarcolemmal regulator MAC, from infarcted area. The recent discovery a rat analogue now allowed first evaluation temporal spatial relationship between component deposition acute infarction (AMI). After ligating left coronary artery rats earliest sign activation, focal C3, observed at 2 hours. Deposition early (C1, C3) late pathway (C8, C9) components AMI lesions occurred 3 Glycophosphoinositol-anchored expressed membranes normal cardiomyocytes. In Western blot analysis extracts heart appeared as band 21 kd molecular weight under nonreducing conditions. Loss association deposits MAC day one onward. results show universally accompanies vivo. It is initiated within hours after obstruction via which may be due generation alternative C3 convertase ischemic C1 also starts during (2 4 hours) ischemia. Subsequent protective antigen initiate postinjury clearance irreversibly damaged tissue.
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