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1 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: mtjiang{at}mcw.edu.
Activation of mitochondrial ATP-sensitive K+ channels (mitoKATP) is critical in myocardial protection induced by preconditioning with volatile anesthetics or brief periods of ischemia. In this study we have characterized rat mitoKATP reconstituted in lipid bilayers and examined their direct regulation by isoflurane. Mitochondria and inner membrane fraction were isolated from rat ventricles and fused into lipid bilayers. Based on their inhibition by 5-hydroxydecanoate (5-HD)/ATP or activation by diazoxide, mitoKATP of several conductance levels were observed in symmetrical (150 mM) potassium glutamate (26, 47, 66, 83 pS, 105 pS). Isoflurane (0.8 mM) increased the cumulative open probability (NPo) from 0.09±0.02 at baseline to 0.50±0.09 (P < 0.05, n=5), which was inhibited by 5-HD. Isoflurane also caused a dose-dependent right-shift in ATP-inhibition of mitoKATP, which increased the IC50 for ATP from 335±4µM to 940±34 µM at 0.8 mM (P < 0.05, n=5~8).We conclude that direct activation of the mitoKATP by isoflurane is likely to contribute to volatile anesthetics-induced myocardial preconditioning.
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