Abstract
The preservation of mitochondrial function after ischemia is involved in the mechanism of anesthetics-induced cardioprotection. Nitric oxide (NO) is recognized as a trigger or mediator of anesthetic-induced pre- and post-conditioning. In the present study, we investigated the modulatory effect of NO on the effect of isoflurane on complex I-linked mitochondrial respiration. Respiration rates were measured in isolated rat heart mitochondria polarographically with a computer-controlled Clark-type O2 electrode using complex I substrates glutamate and malate. To test the involvement of NO on the isoflurane-induced changes of mitochondrial respiration, NO donor SNAP and NO synthase inhibitor L-NIO were added with or without isoflurane (0.25 mM) before ADP initiated state 3 respiration. Isoflurane attenuated state 3 respiration (82±6% of control). L-NIO (10 μM) or SNAP (1 μM) alone had no effect on state 3 respiration (101±7%, 100±5% of control, respectively). In addition, L-NIO and SNAP did not alter the attenuation of isoflurane on state 3 respiration (84±7%, 85±5% of control, respectively). We conclude that isoflurane attenuates mitochondrial state 3 respiratory rate under complex I substrates glutamate and malate. In addition, this effect of isoflurane-induced attenuation of state 3 respiration is independent of mitochondrial NO.
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