1978 Volume 9 Issue 2 Pages 197-201
Effect of increased intravascular coagulation on the digestive mucosa was investigated in an experimental model of DIC (disseminated intravascular coagulation) produced in dogs and rats.
Intravenous administration of bacterial endotoxin caused marked hemorrhagic necrosis of the intestinal mucosa of dogs within 3 to 8 hours, and the lesion was coated with whitish pseudomembrane. Histologically, the villi showed marked deformity, fall of epithelial cells, cellular infiltrations, and sludging of red cells or thrombic formation in the microcirculations. There was no evidence of the increased tissue fibrinolytic activity in the affected mucosa. These data led us to conclude that the intravascular coagulation in the microcirculation of the intestinal mucosa affords to produce hemorrhagic necrosis of the mucosa, and to which fibrinolytic activity does not participate.
Pretreatment of the intestinal mucosa of a dog by trans-AMCHA, a potent antiplasmin compound, or by Trasylol prior to the endotoxin shock, prevented the intestinal mucosa from hemorrhagic necrosis, and it was indicated that proteolytic enzymes present along the intestinal wall played a role in the production of mucosal damage when the microcirculation of the mucosa was disturbed by endotoxin.
Further, it was found that rats treated with trans-AMCHA showed enhancement of the production of intestinal lesions following to the administration of endotoxin, indicating the antiplasmin agent inhibited secondary fibrinolysis and accelerated the clot formation in the rat.
