Experimental gram-negative peritonitis: decreased thromboplastin activity in organs with a simultaneous rise of thromboplastin in blood monocytes and peritoneal macrophages.

Thromboplastin values in blood monocytes, peritoneal macrophages, and in tissue samples from lung, aortic wall, liver, spleen, pancreas, kidney, jejunum, and colon were determined at 4, 10, and 16 h after induction of acute peritonitis (cecal perforation) or sham operation in rats. A maximum 35-fold and 100-fold rise of values was respectively demonstrated in monocytes and peritoneal macrophages in septic animals as compared to controls. This monocyte-macrophage-derived thromboplastin is probably central to the activation of blood coagulation and fibrin depositions/adhesion formation in septic peritonitis. A simultaneous and significant fall in thromboplastin content of standardized specimens from lung, aortic wall, liver, spleen, pancreas, and jejunum was observed in rats with peritonitis. This could reflect mobilization of thromboplastin in favor of the infectious focus. No significant changes were detected in tissue from kidney, whereas samples from the colon of septic animals showed a consistent increase as compared to controls.