Complement-mediated leucoembolization: a mechanism of tissue damage during extracorporeal perfusions, myocardial infarction and in shock--a review.

The complement (C) system evolved as a beneficial antimicrobial system. However, when activated during extracorporeal perfusion as with haemodialysis or cardiopulmonary bypass modest pulmonary dysfunction associated with granulocyte aggregation and embolization can occur. When C activation is massive and prolonged, as with severe sepsis, trauma, or acute pancreatitis, severe pulmonary damage which is recognized as shock lung, or adult respiratory distress syndrome, may occur. Since ulcerating atherosclerotic plaques can also activate C, a mechanism by which myocardial infarcts may extend during the first few hours after infarction is also implied. Therapeutic ramifications of these conclusions are evident. Thus, high doses of corticosteroids or of nonsteroidal anti-inflammatory agents such as ibuprofen share the ability to prevent aggregation and embolization of stimulated granulocytes to patent vessels downstream and also inhibit their production of toxic oxygen radicals. These properties suggest the use of these agents in myocardial infarction and shock states, particularly shock lung, and appropriate clinical trials are awaited with interest.