Potentiation of carbon tetrachloride hepatotoxicity by hypoxia.
To determine the cause of hepatic injury in patients with hypoxaemia, the persistence of liver susceptibility to toxic injury after hypoxia was investigated in rats. Centrilobular necrosis and marked elevation of serum glutamic-pyruvic transaminase (SGPT) and serum glutamic-oxaloacetic transaminase (SGOT) activities were induced by carbon tetrachloride (0.1 ml/kg body weight) given in the period between 3 h before and 21 h after exposure to 7% oxygen for 3 h. This observation, that a short period of hypoxia results in a prolonged sensitivity to carbon tetrachloride-induced liver injury, has not been described previously. The mechanism of the phenomenon is obscure. These observations suggest that the hepatic injury in patients with hypoxaemia may be caused not only by the hypoxia per se or chemicals administered before or during hypoxia, but also by chemicals given within 24 h of hypoxaemia.
D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002251:Carbon Tetrachloride / Q000633:toxicity*; D056486:Chemical and Drug Induced Liver Injury; D008099:Liver / Q000473:pathology; D008107:Liver Diseases / Q000201:enzymology / Q000473:pathology; D008297:Male; D009336:Necrosis; D010100:Oxygen; D051381:Rats; D011919:Rats, Inbred Strains
D002251:Carbon Tetrachloride; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D010100:Oxygen