Abstract
The relationship between disseminated intravascular coagulation (DIC) and reticuloendothelial system (RES) was investigated clinicopathologically using autopsy cases and experimentally in rabbits treated with two injections of endotoxin at an interval of 24 hours. Fibrin thrombi were observed in the liver in 42% of the 14 DIC cases and in the spleen in 35%. There was a tendency of thrombus formation in an earlier phase in the liver and spleen than in other organs. This result was compatible with the experimental one. Kupffer cells and macrophages in DIC cases increased in number and showed an increased phagocytic activity than in the control ones.
In the experimental model, first intravenous injection of endotoxin made RES a more active form with many phagosomes and tiny fibrin threads around them. After the second injection of endotoxin, a great number of fibrin thrombi were observed in the spleen, liver, kidney and lung. The cells of RES showed intimate relationship to fibrin thrombi with the intricate invagination of cytoplasmic membrane engulfing fibrin thrombi. However, no definite evidence of phagocytosis, such as phagolysosomal disposition of fibrin, was observed.
In rabbits in a state of DIC induced by one intravenous injection of endotoxin with pretreatment of intravenous latex injection, features of active fibrin disposition were observed even in swollen macrophages phagocytizing many latex particles. The particles of colloidal iron injected intravenously in the rabbits three hours after the second injection of endotoxin were phagocytized by splenic phagocytes, and its number was greater than that in control rabbits.
These results suggest that the RES activation or hyperfunction rather than its blockade may be more important in the pathogenesis of DIC.
