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Am J Physiol Heart Circ Physiol (February 28, 2002). doi:10.1152/ajpheart.01056.2001
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Articles in PresS, published online ahead of print February 28, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01056.2001
Submitted on December 3, 2001
Accepted on February 26, 2002

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

ENIS NOVALIJA1*, SRINIVASAN G VARADARAJAN2, AMADOU K CAMARA2, JIANZHONG AN2, QUN CHEN2, MATTHIAS L RIESS2, NEIL HOGG3, and DAVID F STOWE4

1 Anesthesiology, Medical College of Wisconsin/Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin, USA; Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
2 Anesthesiology, Medical College of Wisconsin/Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin, USA
3 Biophysics Research Institute, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
4 Anesthesiology, Medical College of Wisconsin/Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin, USA; Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA; Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, Wisconsin, USA

* To whom correspondence should be addressed. E-mail: novalija{at}mcw.edu.

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 reactive oxygen and nitrogen species to form strong oxidants, principally peroxynitrite (ONOO-) and then forms fluorescent dityrosine. ROS scavengers superoxide dismutase, catalase and glutathione (SCG), and NO. synthesis inhibitor L-NAME (LNA) were given 5 min before and after sevoflurane preconditioning stimuli. Drugs were washed out before 30 min of ischemia and 120 min reperfusion. Groups were CON (non-treated ischemia control), APC (two, 2-min periods of perfusion with 0.32 ± 0.02 mM of sevoflurane; separated by a six min period of perfusion without sevoflurane), SCG, APC+SCG, LNA, and APC+LNA; effluent dityrosine at 1 min reperfusion was 56±6 (SEM)*, 15±5, 40±5*, 39±4*, 35±4*, 33±5* units (*p <0.05 vs APC), respectively; LVP (% baseline) at 60 min reperfusion was 30±5*, 60±4, 35±5*, 37±5*, 44± 4, 47±4; infarct size was 50±5*, 19±2, 48±3*, 46±4*, 42±4*, 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.




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