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Articles in PresS, published online ahead of print March 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01057.2001
Submitted on December 3, 2001
Accepted on March 8, 2002
1 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA; Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA; Department of Anesthesiology and Intensive Care Medicine, University Hospital Munster, Munster, Germany
2 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
3 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA; Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
4 Department of Biomedical Engineering, Marquette University, Milwaukee, Wisconsin, USA
5 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA; Department of 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: mriess{at}mcw.edu.
NADH increases during ischemia because O2 shortage limits NADH oxidation at the electron transport chain. Ischemic (IPC) and anesthetic preconditioning (APC) attenuate cardiac reperfusion injury. We examined if IPC and APC similarly alter NADH, i.e. mitochondrial metabolism. NADH fluorescence was measured at the left ventricular wall of 40 Langendorff-prepared guinea pig hearts. IPC was achieved by two 5-min periods of ischemia, and APC by exposure to 0.5 or 1.3 mM sevoflurane for 15 min, each ending 30 min prior to 30 min global ischemia. During ischemia, NADH initially increased in non-preconditioned control hearts, then gradually declined below baseline levels. This increase in NADH was lower after APC but not after IPC. The subsequent decline was slower after IPC and APC. On reperfusion, NADH was less decreased after IPC or APC, mechanical and metabolic functions were improved, and infarct size was lower compared to controls. Our results indicate that IPC and APC cause distinctive changes in mitochondrial metabolism during ischemia, and thus lead to improved function and tissue viability on reperfusion.
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