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Anesthetic preconditioning: triggering role of reactive oxygen and nitrogen species in isolated hearts

2002; American Physical Society; Volume: 283; Issue: 1 Linguagem: Inglês

10.1152/ajpheart.01056.2001

1522-1539

Enis Novalija, Srinivasan G. Varadarajan, Amadou K.S. Camara, Jianzhong An, Qun Chen, Matthias L. Riess, Neil Hogg, David F. Stowe,

Anesthesia and Neurotoxicity Research

We postulated that anesthetic preconditioning (APC) is triggered by reactive oxygen/nitrogen species (ROS/RNS). We used the isolated guinea pig heart perfused withl-tyrosine, which reacts with ROS and RNS to form strong oxidants, principally peroxynitrite (ONOO − ), and then forms fluorescent dityrosine. ROS scavengers superoxide dismutase, catalase, and glutathione (SCG) and NO· synthesis inhibitor N G -nitro-l-arginine methyl ester (l-NAME) were given 5 min before and after sevoflurane preconditioning stimuli. Drugs were washed out before 30 min of ischemia and 120 min of reperfusion. Groups were control (nontreated ischemia control), APC (two, 2-min periods of perfusion with 0.32 ± 0.02 mM of sevoflurane; separated by a 6-min period of perfusion without sevoflurane), SCG, APC + SCG,l-NAME, and APC + l-NAME. Effluent dityrosine at 1 min reperfusion was 56 ± 6 (SE)‡, 15 ± 5, 40 ± 5‡, 39 ± 4‡, 35 ± 4‡, and 33 ± 5‡ units (‡ P < 0.05 vs. APC), respectively; left ventricular pressure (%baseline) at 60 min of reperfusion was 30 ± 5‡, 60 ± 4, 35 ± 5‡, 37 ± 5‡, 44 ± 4, and 47 ± 4; and infarct size (%total heart weight) was 50 ± 5‡, 19 ± 2, 48 ± 3‡, 46 ± 4‡, 42 ± 4‡, and 45 ± 2‡. Thus APC is initiated by ROS as shown by improved function, reduced infarct size, and reduced dityrosine on reperfusion; protective and ROS/RNS-reducing effect of APC were attenuated when bracketed by ROS scavengers or NO· inhibition.