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Anesthesiology Research Laboratory, Departments of 1 Anesthesiology and 2 Physiology, and 3 Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee 53226; 4 Department of Biomedical Engineering, Marquette University, Milwaukee 53233; 5 Research Service, Veterans Affairs Medical Center, Milwaukee, Wisconsin 53295; and 6 Department of Anesthesiology and Intensive Care Medicine, University Hospital Münster, 48129 Münster, Germany
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 whether 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 before 30 min of global ischemia. During ischemia, NADH initially increased in nonpreconditioned control hearts and 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 with 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.
experimental; infarction; sevoflurane; dose dependency; mitochondrial function
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