Effects of volatile anesthetics on myocardial oxidation-reduction status assessed by NADH fluorometry.
In experiments on isolated rat heart perfused by the Langendorff method, the effect of halothane, isoflurane, enflurane, and diethyl ether on myocardial oxidation-reduction status was evaluated with reduced nicotinamide adenine dinucleotide (NADH) fluorometry. All inhaled anesthetics studied caused a dose-dependent increase in NADH fluorescence. Concentrations of anesthetics necessary to produce 10% of the maximal increase in NADH fluorescence caused by anoxia were 1.1% for halothane, 1.6% for isoflurane, 2.6% for enflurane, and 6.8% for diethyl ether (all concentrations are different from each other at P less than 0.05 level, n = 24). These findings indicate that the order of potency with regard to the effect of the agent on NADH paralleled their potencies as general anesthetics. The deterioration in myocardial oxidation-reduction status probably is related to the ability of the anesthetic agents to inhibit the electron transport chain in mitochondria.
D000777:Anesthetics / Q000494:pharmacology*; D000818:Animals; D004737:Enflurane / Q000494:pharmacology; D005470:Fluorometry; D006221:Halothane / Q000494:pharmacology; D007530:Isoflurane / Q000494:pharmacology; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D009243:NAD; D010424:Pentobarbital / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013874:Thiopental / Q000494:pharmacology; D014835:Volatilization
D000777:Anesthetics; D009243:NAD; D004737:Enflurane; D007530:Isoflurane; D010424:Pentobarbital; D013874:Thiopental; D006221:Halothane