[Metabolism of halothane in rats with CCl4-alcohol-induced liver fibrosis].
Rats treated with carbon tetrachloride (CCl4, twice weekly 0.2 ml/kg p.o.) and a 5% ethanol solution instead of drinking water developed a marked fibrosis and steatosis of the liver within 4 weeks. Fibrosis was evidenced by a 7-fold increase in the hepatic hydroxyproline content and steatosis by a 3-fold increase in the triglyceride content. Exposing these rats to a non-narcotic concentration of halothane (100 ppm) in a closed system the metabolic removal of the anesthetic from the atmosphere of the system was measured. In control rats treated with olive oil and water the elimination half-life for halothane amounted to 0,78 (0,69-0.88) h (confidence limits for p = 0.95). In rats with CCl4-ethanol-induced liver fibrosis and steatosis this elimination half-life was prolonged to 1.24 (1.07-1.41) h indicating an impaired metabolic degradation of halothane in these rats.
D000818:Animals; D001711:Biotransformation; D002252:Carbon Tetrachloride Poisoning / Q000378:metabolism*; D006221:Halothane / Q000378:metabolism*; D006909:Hydroxyproline / Q000378:metabolism; D007700:Kinetics; D008104:Liver Cirrhosis, Alcoholic / Q000378:metabolism*; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000378:metabolism*; D008297:Male; D009929:Organ Size; D051381:Rats; D011919:Rats, Inbred Strains; D014280:Triglycerides / Q000378:metabolism
D014280:Triglycerides; D006909:Hydroxyproline; D006221:Halothane
Metabolismus von Halothan bei Ratten mit CCl4-alkoholinduzierter Leberfibrose.