The Role of Complement in Endotoxin‐Induced Disseminated Intravascular Coagulation: Studies in Congenitally C 6 ‐Deficient Rabbits

S ummary . The effect of intravenous infusion of endotoxin on the activation of intravascular coagulation and on the generation of glomerular microclots was studied in rabbits congenitally deficient in the sixth component of complement (C 6 ). Endotoxin infusion induced the formation of circulating soluble fibrin and caused a drop in leucocyte and platelet counts, a decrease in factor‐V and factor‐VII activities and a prolongation of the thromboplastin time as well as the partial thromboplastin time. These haematological changes are indicative of consumption coagulopathy and were similarly distinctive in C 6 ‐deficient as in normal rabbits infused with endotoxin. Furthermore, renal glomerular microclots formed in 90% of the C 6 ‐deficient and in 80% of the normal rabbits after endotoxin administration. The haematological as well as the histological results of these experiments demonstrate that the sixth component of complement and the later complement components C 7–9 are not essential to the initiation of intravascular coagulation by endotoxin and the manifestation of the generalized Shwartzman reaction. The data make it likely that the release of platelet factor 3 does not represent the trigger mechanism of intravascular coagulation since disseminated intravascular coagulation could be induced in C 6 ‐deficient rabbits although the platelets of these animals are incapable of releasing platelet factor 3 activity after platelet‐endotoxin interaction.