[Characteristics of the ischemic disorders of xenobiotic metabolism in the liver of rats in the early and late stages of recovery].
It has been demonstrated in rat experiments that total ischemia of the liver leads to disorders of the metabolism of xenobiotics and endogenous substrates. Upset hexenal metabolism manifests in the prolongation of the hexenal-induced sleep and hexenal concentration elevation in blood plasma for 18 days of the postischemic period. Following exposure to ischemia liver microsomes show a decrease in the rate of amidopyrine, aniline and hydrocortisone hydroxylation. Hydrocortisone metabolism returns to normal by day 14, that of amidopyrine by day 21 of the postischemic period. Aniline metabolism gets disturbed to a greater degree, remaining 33.4% lower by day 21. It has been shown that the inducibility of microsomal monooxygenases is substantially restricted by days 7 and 14 of the postischemic period.
D000632:Aminopyrine / Q000097:blood*; D000814:Aniline Compounds / Q000378:metabolism*; D000818:Animals; D004790:Enzyme Induction / Q000187:drug effects; D006591:Hexobarbital / Q000097:blood*; D006854:Hydrocortisone / Q000378:metabolism*; D066298:In Vitro Techniques; D007511:Ischemia / Q000201:enzymology*; D008099:Liver / Q000098:blood supply* / Q000201:enzymology; D008297:Male; D008862:Microsomes, Liver / Q000201:enzymology; D010088:Oxidoreductases / Q000096:biosynthesis; D010634:Phenobarbital / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D000814:Aniline Compounds; D000632:Aminopyrine; D006591:Hexobarbital; D010088:Oxidoreductases; C023650:aniline; D006854:Hydrocortisone; D010634:Phenobarbital
Kharakteristika ishemicheskikh narusheniĭ metabolizma ksenobiotikov v pecheni krys na rannikh i otdalennykh étapakh vosstanovleniia.