Premium
Nitric oxide is not involved in the attenuation of complex I‐linked mitochondrial state 3 respiration by isoflurane
Author(s) -
An Jianzhong,
Camara Amadou KS,
Bienengraeber Martin,
Bosnjak Zeljko J
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a863-a
Subject(s) - isoflurane , respiration , mitochondrion , nitric oxide , chemistry , biochemistry , pharmacology , anesthesia , biology , medicine , anatomy , organic chemistry
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 O 2 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.