Stroma Activation

The syndrome of disseminated intravascular coagulation (DIC) 1 is a recognized complication of acute hemolytic episodes in both man (1-3) and laboratory animals (4, 5) and has been induced experimentally in monkeys and dogs by infusion of autologous red blood cell stroma (6, 7). The mechanism of stromainduced D I C may be analogous to the demonstrable procoagulant activity of red cell membrane phospholipids in vitro. However, an additional or alternative chain of events involving activation of the complement system is suggested by the well-studied model of DIC , the Sanarelli-Shwartzman reaction, produced by two appropriately spaced intravenous injections of bacterial endotoxin. The recent work of Fong and Good (8) and Margaret ten (9) indicate a requirement for platelets and an intact complement system for endotoxin-induced DIC. Complement activation by endotoxin proceeds primarily, if not entirely, via the recently described alternate pathway (10). In view of the ultrastructural similarity between endotoxin and red cell stroma (i.e., bilaminar membrane [11]) and their ability to produce DIC, we have initiated studies to determine whether red cell stroma is also capable of activating the alternate complement pa thway and to a t tempt to relate this function to the sequence of events leading to DIC.