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From the Departments of *Anesthesiology, and Internal Medicine, Osaka Dental University, Osaka, Japan; and Institute for Heart and Vascular Health, Albert Einstein Medical Center, Philadelphia, Pennsylvania.
Address correspondence and reprint requests to Masami Miyamae, MD, PhD, Department of Internal Medicine, Osaka Dental University, 8-1 Kuzuha hanazono-cho Hirakata, Osaka 573-1121, Japan. Address e-mail to kyotomiya{at}hotmail.com.
Abstract
BACKGROUND: Volatile anesthetics and regular ethanol consumption induce cardioprotection mimicking ischemic preconditioning. We investigated whether sevoflurane enhances ethanol preconditioning and whether inhibition of protein kinase C (PKC) and mitochondrial KATP channels attenuated this enhanced cardioprotection. The effects of regular ethanol consumption on expression of inducible (iNOS) and endothelial (eNOS) nitric oxide synthase were determined.
METHODS: Isolated perfused guinea pig hearts underwent 30-min global ischemia and 120-min reperfusion (Control: CTL). The ethanol group (EtOH) received 2.5% ethanol in their drinking water for 6 wk. Anesthetic preconditioning was elicited by 10-min exposure to sevoflurane (1 minimum alveolar anesthetic concentration; 2%) in ethanol (EtOH + SEVO) or nonethanol (SEVO) hearts. PKC and mitochondrial KATP channels were inhibited with chelerythrine and 5-hydroxydecanoate pretreatment, respectively. Contractile recovery was assessed by monitoring of left ventricular developed and end-diastolic pressures. Infarct size was determined by triphenyltetrazolium chloride staining. Expression of iNOS and eNOS were determined by Western blot analysis.
RESULTS: After ischemia-reperfusion, hearts from the EtOH, sevoflurane (SEVO), and EtOH + SEVO groups had higher left ventricular developed pressure and lower left ventricular end-diastolic pressure compared with CTL. Infarct size was reduced in EtOH and SEVO hearts compared with CTL (27% and 23% vs 45%, respectively, P < 0.001). Sevoflurane further reduced infarct size in EtOH hearts (27% vs 15%, P < 0.001). Chelerythrine and 5-hydroxydecanoate abolished cardioprotection in both SEVO and EtOH cardioprotected hearts. iNOS expression was reduced and eNOS expression was increased in EtOH hearts.
CONCLUSIONS: Sevoflurane enhances cardiac preconditioning induced by regular EtOH consumption. This effect is mediated in part by modulation of PKC and mitochondrial KATP channels, and possibly by altered modulation of NOS expression.
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  P. S. Pagel Additive Cardioprotection by Ethanol and Sevoflurane: Are Sarcolemmal KATP Channels Also Involved? Anesth. Analg., June 1, 2008; 106(6): 1926 - 1926. [Full Text] [PDF]
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