The role of hepatic venous congestion and endotoxaemia in the production of fulminant hepatic failure secondary to congestive heart failure.

The present study was undertaken to clarify the role of congestion of the liver and endotoxemia in the production of fulminant hepatic failure secondary to congestive heart failure. Induction of congestion of the liver, i.e. an elevation of hepatic venous pressure, in rats was accomplished by partial obstruction of the inferior vena cava. A close relationship was demonstrated between venous pressure and serum levels of transaminases as a measure of hepatic dysfunction. Hepatic dysfunction was mild in rats with venous hypertension alone, and only centrilobular congestion was seen on microscopy. In contrast, severe abnormalities of hepatic function were induced by venous hypertension and endotoxaemia. Histologically, the liver revealed bridging centrilobular necrosis as seen in patients with congestive heart failure who develop fulminant hepatic failure. These data suggest that coexistence of endotoxaemia and congestion of the liver may induce fulminant hepatic failure, and that the latter alone is associated only with slight hepatic dysfunction and liver damage.