The neutrophil chemotaxis was measured in 25 cases of disseminated intravascular coagulation syndrome (DIC) by the agarose plate method using 3 kinds of chemotaxins, Zymosan activated serum (ZAS), Bacterial culture filtrates (BCF) and N-formyl-1-methionyl-1-phenylalanine (FMP).
Different results were obtained depending on the pathogenesis of DIC. In the DIC due to sepsis and other diseases than liver cirrhosis, either chemotaxis or random mobility significantly decreased, especially, the chemotaxis to complement-derived chemotaxin, i.e. ZAS. On the otherhand, both chemotaxis and random mobility were normal in the DIC developing in patients with liver cirrhosis.
In the sepsis-derived DIC, the neutrophil chemotaxis tended to associate with the levels of antithrombin III, plasminogen and serum CH50. In one case of sepsis-derived DIC, the neutrophil chemotaxis changed parallel to the severity of DIC.
Endotoxin was frequently demonstrated in the sepsis-derived DIC. As the endotoxin is known to activate the complement system in the blood, it is proposed that the impairment of neutrophil chemotaxis in the sepsis-derived DIC can be due to the chemotactic deactivation of neutrophils, which have come in contact with complement-derived chemotaxin resulting from intravascular complement activation by endotoxin.
