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LETTER TO THE EDITOR

Additive Cardioprotection by Ethanol and Sevoflurane: Are Sarcolemmal K_ATP Channels Also Involved?

Department of Internal Medicine and Anesthesiology; Osaka Dental University Osaka, Japan; kyotomiya{at}hotmail.com (Miyamae, Sugioka) Institute for Heart and Vascular Health; Albert Einstein Medical Center; Philadelphia, Pennsylvania (Figueredo)

In Response:

We thank Dr. Pagel for an excellent summary of the potential role of sarcolemmal KATP channels (sarcK_ATP) in the preconditioning-like effect of both chronic ethanol consumption and volatile anesthetics.1 We also have been working to understand the signaling cascade mediating the cardioprotection that we first described chronic ethanol consumption to have against ischemia–reperfusion injury (and more recently the protection afforded by volatile anesthetics).2,3 We did limit our study to the potential role of mitochondrial KATP channels (mitoK_ATP) in mediating the additive preconditioning effects of chronic ethanol and sevoflurane. Our previous study demonstrating the translocation of protein kinase C from the cytosol to the myofibrils in myocytes taken from Guinea pigs chronically exposed to ethanol led us to pursue the potential role of mitoK_ATP in mediating this additive cardioprotection.4 However, as Dr. Pagel has demonstrated, there may be a role for both sarcK_ATP and mitoK_ATP in mediating the additive cardioprotective effects of chronic ethanol and volatile anesthetics. Of note, we reported that chronic ethanol consumption increased eNOS expression. NO has been shown to activate sarcK_ATP through a cGMP- dependent mechanism.5,6 As we try to understand the signaling cascade that ultimately leads to these preconditioning-like effects, the role of sarcK_ATP will need to be considered.

REFERENCES

1. Paul S. Pagel. Additive cardioprotection by ethanol and sevoflurane: are sarcolemmal K_ATP channels also involved? Anesth Analg 2008;106:1926[Free Full Text]
2. Miyamae M, Diamond I, Weiner MW, Camacho SA, Figueredo VM. Regular alcohol consumption mimics cardiac preconditioning by protecting against ischemia-reperfusion injury. Proc Natl Acad Sci USA 1997;94:3235–9[Abstract/Free Full Text]
3. Miyamae M, Camacho SA, Zhou HZ, Diamond I, Figueredo VM. Alcohol consumption reduces ischemia-reperfusion injury by species-specific signaling in guinea pigs and rats. Am J Physiol Heart Circ Physiol 1998;275:H50–H56[Abstract/Free Full Text]
4. Miyamae M, Rodriguez MM, Camacho SA, Diamond I, Mochly-Rosen D, Figueredo VM. Activation of protein kinase C correlates with a cardioprotective effect of regular ethanol consumption. Proc Natl Acad Sci USA 1998;95:8262–7[Abstract/Free Full Text]
5. Han J, Kim N, Joo H, Kim E, Earm YE. ATP-sensitive K(+) channel activation by nitric oxide and protein kinase G in rabbit ventricular myocytes. Am J Physiol Heart Circ Physiol 2002;283:H1545–H1554[Abstract/Free Full Text]
6. Cuong DV, Kim N, Youm JB, Joo H, Warda M, Lee JW, Park WS, Kim T, Kang S, Kim H, Han J. Nitric oxide-cGMP-protein kinase G signaling pathway induces anoxic preconditioning through activation of ATP-sensitive K+ channels in rat hearts. Am J Physiol Heart Circ Physiol 2006;290:H1808–H1817[Abstract/Free Full Text]

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