Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhibition of an increase in total content of unsaturated fatty acids in microsomal lipids induced by phenobarbital, alterations of parameters of the fluorescent probe 1,8-ANS-binding with membranes as well as restrictions in induction of liver microsomal monooxygenase enzymatic system were detected during postischemic period after total liver tissue ischemia. Preadministration of alpha-tocopherol and lidocaine prevented distinctly the structure-functional alterations induced by phenobarbital in liver microsomal membranes during postischemic period. Possible factors responsible for limitations of the phenobarbital inducing effect during postischemic period are discussed.
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PMID:[The effect of alpha-tocopherol and lidocaine on the structural-functional rearrangement of liver endoplasmic reticulum membranes after induction with phenobarbital in the postischemic period]. 236 49

A previously validated small mammal trauma model, hind-limb ischemia secondary to infrarenal aortic ligation in the rat, was utilized to further investigate the effects of traumatic injury on the hepatic cytochromes P-450. In vitro drug metabolism studies with hexobarbital and zoxazolamine as substrates confirmed the post-traumatic depression of the cytochrome P-450-catalyzed oxidation of these drugs which was suggested by previous in vivo pharmacokinetic studies. Enzyme kinetic studies revealed diminished Vmax values with no change in Km, a finding which would seem to concur with the previously demonstrated decrease in hepatic cytochrome P-450 content after model trauma. Moreover, a battery of in vitro microsomal monooxygenase assays demonstrated that model trauma exerted a differential effect on various hepatic cytochrome P-450 isoenzymes. This phenomenon was confirmed by anion-exchange HPLC of solubilized hepatic microsomal hemoproteins. One of the most interesting aspects of this selective effect on cytochrome P-450 subtypes was the relative induction of cytochrome P-448 content and activity, in contrast to the variable decrease seen with cytochrome P-450 activities. The potential in vivo sequelae of this differential influence were suggested by changes observed in the urinary metabolic profile of antipyrine after model trauma.
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PMID:Effects of model traumatic injury on hepatic drug metabolism in the rat. III. Differential responses of cytochrome P-450 subpopulations. 614 9