Neutrophil activation as a mechanism of tissue injury.
C5A is capable of causing granulocyte/granulocyte interactions that lead to clumping, vasoocclusion, and the extension of infarctive damage in patients with coronary artery disease. Employing a new rheologic procedure, laser transillumination of thin vascular beds, one directly observes in vivo granulocyte aggregation in the mesentery of the rat. Nonsteroidal antiinflammatory drugs (NSAIDs) were shown to stop granulocyte agglomeration and to limit the extension of experimental myocardial infarcts in the cat. There may be application for NSAIDs for myocardial infarction in humans. NSAIDs block granulocyte aggregation to both a traditional activated complement and a complement activated by cryoglobulins. Patients with severe cryoglobulinemic cutaneous vasculitis who failed on steroids responded to NSAID administration.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002415:Cats; D002449:Cell Aggregation / Q000187:drug effects; D003167:Complement Activation; D003182:Complement C5 / Q000276:immunology; D015936:Complement C5a; D003450:Cryoglobulins / Q000276:immunology; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy / Q000276:immunology; D009504:Neutrophils / Q000276:immunology*; D051381:Rats; D014657:Vasculitis / Q000188:drug therapy / Q000276:immunology*
D000893:Anti-Inflammatory Agents; D003182:Complement C5; D003450:Cryoglobulins; D015936:Complement C5a