CHOLESTEROL AND ATHEROMA LIPIDS ACTIVATE COMPLEMENT AND STIMULATE GRANULOCYTES - A POSSIBLE MECHANISM FOR AMPLIFICATION OF ISCHEMIC-INJURY IN ATHEROSCLEROTIC STATES

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  • 1 January 1981
    • journal article
    • research article
    • Vol. 98  (1) , 68-77
Abstract
Studies in experimental myocardial infarction have suggested that PMN [granulocytes] and plasma C [complement] might interact to intensity ischemic injury. From the finding of large amounts of activated C (specifically C5a) in the plasma of a patient with severe, ulcerating atherosclerosis and the cholesterol embolization syndrome, crystalline cholesterol was postulated to activate C and thereby amplify infarctive tissue damage. On simple incubation, crystalline cholesterol, and lipids from atheromata, activated plasma C; such plasma then potently aggregated normal PMN and provokedthem to damage cultured endothelial cells in vitro. The active principle in cholesterol-incubated plasma was a molecular weight and antigenicity consistent with C5a (or C5a[desarginine]). Optimal activation required the presence of Ig and an intact classical C pathway. Exposure of plasma to crystalline cholesterol by ulceration of, or hemorrhage into, atherosclerotic plaques might therefore activate C in vivo, promoting further ischemic damage by causing leukostatic-leukoembolic compromise of small vessels downstream from the site of activation.