| ||||||||||||||
|
|
|||||||||||||
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 (sarcKATP) 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 (mitoKATP) 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 mitoKATP in mediating this additive cardioprotection.4 However, as Dr. Pagel has demonstrated, there may be a role for both sarcKATP and mitoKATP 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 sarcKATP 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 sarcKATP will need to be considered.
REFERENCES
protein kinase C correlates with a cardioprotective effect of regular ethanol consumption. Proc Natl Acad Sci USA 1998;95:8262–7
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||
|