Role of endotoxaemia in the development of hepatic failure following hepatic artery occlusion

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Abstract
The present study was undertaken to examine whether endotoxaemia relates to the development of hepatic failure following surgical ligation or embolization of the hepatic artery. A small amount of endotoxin was given immediately or 1 week after hepatic artery ligation in rats, and liver function tests and morphological examination of the liver were performed at 24 h after the administration. Hepatic artery ligation alone or endotoxin administration alone did not induce functional and morphological alteration of the liver. However, when endotoxin was given immediately after hepatic artery ligation, there was an increase in serum transaminase activity and focal hepatocellular necrosis developed. On the other hand, when endotoxin was given 1 week after hepatic artery ligation, the hepatic injury was not induced because of the development of hepatic arterial collaterals. These data suggest that endotoxaemia may be a cause of hepatic failure following hepatic artery occlusion, and that the risk may persist until the establishment of hepatic arterial collaterals.