Influence of hemorrhagic shock on hepatic energy metabolism in carbon tetrachloride-induced cirrhotic rats.

The influence of hemorrhagic shock on hepatic energy metabolism was investigated in carbon tetrachloride (CCl4)-induced cirrhotic rat. In normal and CCl4-treated rats, the hepatic mitochondrial redox state and phosphorylative activity decreased significantly (P less than 0.001) following hemorrhagic shock, with mean arterial blood pressure at 30 mmHg. In normal rats, they were immediately restored upon reinfusion of shed blood after 2 hr of hemorrhagic shock, followed by marked enhancement 120 min later. By contrast, in cirrhotic rats redox state and phosphorylative activity in hepatic mitochondria did not recover immediately, and there was neither elevation of redox state nor enhancement of phosphorylative activity in hepatic mitochondria. The survival rate at 24 hr was 10% in contrast to 90% in normal rats. These results suggest that the absence of early recovery followed by enhancement of mitochondrial function in the cirrhotic liver is fundamentally related to the mechanism of hepatic failure following hemorrhagic shock.