The hepatic response to endotoxin shock; Hemodynamic and enzymatic observations

Abstract

In order to evaluate the role of the liver in endotoxin shock, purified endotoxin was injected into the portal vein or into the systemic circulation in dogs. Systemic administration of endotoxin produces a more severe hypotension than does injection into the portal vein, which suggests that endotoxin may be removed from the circulation and detoxified by the hepatic RE system. When the liver was excluded from the circulation, profound hypoglycemia followed administration of endotoxin and death soon occurred. Circulating SGOT, SGPT, and alkaline phosphatase levels increased greatly after administration of endotoxin in dogs with normal hepatic circulation, but the blood LDH levels were higher in dogs in which the hepatic inflow was excluded, which suggests an extrahepatic origin of the LDH isoenzymes. Although the present studies suggest that the liver exerts a protective effect during the initial phase of endotoxin shock, it is believed that with progression of shock the liver deteriorates and hepatic intracellular metabolites may be released into the circulation to accelerate the irreversibility of shock.