[Swelling and loss of potassium in perfused livers following the influence of the vapours of carbon tetrachloride, chloroform and halothane on the perfusion medium (author's transl)].
Erythrocyte free perfused rat livers were treated with vaporous carbon tetrachloride, chloroform and halothane by equilibration in the oxygenator system. The potassium loss, the amount of swelling and the alteration of the perfusion rates were measured during the experiments as criteria of acute toxicity. In contrast to the well known behaviour of perfused livers during the intoxication with phalloidin the amount of liver swelling did not marekdly depend on the perfusion rates in acute CCl(4) poisoning. The mechanism of swelling must be different in both intoxications. Exposure of perfused livers to high concentrations of CCl(4) for several minutes only produced a marked K-+-loss within a short time. This injury could not be fully compensated after finishing the exposure. Dose response diagrams are presented for carbon tetrachloride, chloroform and halothane by use of the following criteria: potassium loss, swelling (increase of wet weight) and perfusion rates (ml.min-1.g-1). As total doses the amounts of solutes vaporized during the exposition were listed. In these diagrams chloroform appears to be more toxic than halothane. CCl4 occupies a middle position between chloroform and halothane. The course of dose response diagrams of halothane is different from those of CCl(4) and CHCl(3). The halothane diagrams increase critically at high doses, whereas the courves for CCl(4) and CHCl(3) rise continuously. With respect to effects on the hepatic microcirculation halothane seems to be less toxic than CCl(4). The results are discussed on the basis of the periods of exposition and the maximal concentrations of the solutes in the perfusion medium. With respect to these data CCl(4) is much more toxic than CHCl(3) and halothane. On the other hand there is no marked difference in acute hepatotoxicity between CHCl(3) and halothane.
D000208:Acute Disease; D000818:Animals; D001487:Basidiomycota; D002251:Carbon Tetrachloride / Q000494:pharmacology*; D002252:Carbon Tetrachloride Poisoning / Q000378:metabolism; D002725:Chloroform / Q000494:pharmacology* / Q000506:poisoning; D004305:Dose-Response Relationship, Drug; D006221:Halothane / Q000494:pharmacology* / Q000506:poisoning; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008102:Liver Circulation / Q000187:drug effects; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D009183:Mycotoxins / Q000506:poisoning; D010477:Perfusion; D011041:Poisoning / Q000378:metabolism / Q000503:physiopathology; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D014241:Trichloroethylene / Q000494:pharmacology
D009183:Mycotoxins; D014241:Trichloroethylene; D002725:Chloroform; D002251:Carbon Tetrachloride; D011188:Potassium; D006221:Halothane
Schwellung und Kaliumverlust bei perfundierten Lebern nach Einwirkung von dampfförmigem Tetrachlorkohlenstoff, Chloroform und Halothan auf das Perfusionsmedium