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Effects of Volatile Anesthetics on Myocardial Oxidation-reduction Status Assessed by NADH Fluorometry
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1983
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Cardiac AnaesthesiaAnesthetic MechanismPharmacotherapyCardiovascular ToxicityRedox BiologyOxidative StressAnesthesiaMyocardial Oxidation-reduction StatusToxicologyCardiologyAnesthetic PharmacologyNadh FluorometryVolatile AnestheticsNadh FluorescencePharmacologyElectron Transport ChainAnaesthetic AgentPhysiologyMetabolismMedicineIsolated Rat HeartAnesthesiology
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.