In this paper we will review data that support the role of complement-granulocyte interactions in ischemic manifestations of atherosclerosis. The possibility that such interactions may aggravate coronary ischemia is suggested by several past observations. First, C activation has been documented during acute myocardial infarction in many patients; this may occur through release of mitochondrial membranes from damaged myocardial cells since such membranes have been shown to activate the complement cascade through the classical pathway. Secondly, if animals are decomplemented before experimental infarction, they suffer smaller infarcts. Finally, the rapid accumulation of granulocytes at sites of experimental infarction has been shown to be due to local C activation and fails to occur in decomplemented animals.
|Original language||English (US)|
|Number of pages||6|
|Journal||Transactions of the Association of American Physicians|
|State||Published - Dec 1 1979|