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Am J Physiol Heart Circ Physiol 283: H44-H52, 2002. First published February 28, 2002; doi:10.1152/ajpheart.01056.2001
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Vol. 283, Issue 1, H44-H52, July 2002

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

Enis Novalija1,2, Srinivasan G. Varadarajan1, Amadou K. S. Camara1, Jianzhong An1, Qun Chen1, Matthias L. Riess1, Neil Hogg3, and David F. Stowe1,2,4,5

Departments of 1 Anesthesiology and 2 Physiology, 3 Biophysics Research Institute, and 4 Cardiovascular Research Center, Medical College of Wisconsin 53226, and 5 Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53295

We postulated that anesthetic preconditioning (APC) is triggered by reactive oxygen/nitrogen species (ROS/RNS). We used the isolated guinea pig heart perfused with L-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 NG-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)Dagger , 15 ± 5, 40 ± 5Dagger , 39 ± 4Dagger , 35 ± 4Dagger , and 33 ± 5Dagger units (Dagger P < 0.05 vs. APC), respectively; left ventricular pressure (%baseline) at 60 min of reperfusion was 30 ± 5Dagger , 60 ± 4, 35 ± 5Dagger , 37 ± 5Dagger , 44 ± 4, and 47 ± 4; and infarct size (%total heart weight) was 50 ± 5Dagger , 19 ± 2, 48 ± 3Dagger , 46 ± 4Dagger , 42 ± 4Dagger , and 45 ± 2Dagger . 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.

guinea pig; experimental; pathophysiology; contractile function; infarct size


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