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Am J Physiol Heart Circ Physiol (January 14, 2005). doi:10.1152/ajpheart.01124.2004
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Submitted on November 8, 2004
Accepted on January 8, 2005

Warm ischemic preconditioning improves mitochondrial redox balance during and after mild hypothermic ischemia in guinea pig isolated hearts

Jianzhong An1, Amadou K. S Camara1, Samhita S Rhodes1, Matthias L Riess2, and David F Stowe3*

1 Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
3 Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Physiology, Medical College of Wisconsin, Milwaukee, WI, USA; Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, WI, USA

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

Ischemic preconditioning (IPC) induces distinctive changes in mitochondrial bioenergetics during warm (37°C) ischemia and improves function and tissue viability on reperfusion. We examined if IPC before 2 h, 27°C hypothermic ischemia affords additive cardioprotection and improves mitochondrial redox balance assessed by mitochondrial NADH and FAD autofluorescence in intact hearts. A mediating role of KATP channel opening was investigated. NADH and FAD fluorescence were measured in the left ventricular wall of guinea pig isolated hearts assigned into five groups (n = 8 each): hypothermia alone, hypothermia with ischemia, IPC with cold ischemia, 5-HD alone, and 5-HD with IPC and cold ischemia. IPC was two 5 min periods of warm global ischemia spaced 5 min apart and 15 min reperfusion before 2 h, 27°C ischemia and 2 h warm reperfusion. The KATP channel inhibitor 5 hydroxydecanoate (5-HD) was perfused from 5 min before until 5 min after IPC. IPC before 2 h, 27°C ischemia led to better recovery of function and lesser tissue damage on reperfusion compared to 27°C ischemia alone. These improvements were preceded by attenuated increases in NADH and decreases in FAD during cold ischemia, and the reverse changes that occurred during warm reperfusion. 5-HD blocked each of these changes induced by IPC. This study indicates that IPC induces additive cardioprotection with mild hypothermic ischemia by improving mitochondrial bioenergetics during and after ischemia. Since effects of IPC on subsequent changes in NADH and FAD were inhibited by 5-HD, this suggests that mitochondrial KATP channel opening plays a substantial role in improving mitochondrial bioenergetics throughout mild hypothermic ischemia and reperfusion.




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