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CARDIOVASCULAR ANESTHESIOLOGY

Sevoflurane Enhances Ethanol-Induced Cardiac Preconditioning Through Modulation of Protein Kinase C, Mitochondrial K_ATP Channels, and Nitric Oxide Synthase, in Guinea Pig Hearts

Kazuhiro Kaneda, DDS^*, Masami Miyamae, MD, PhD, Shingo Sugioka, DDS, PhD^*, Chika Okusa, DDS^*, Yoshitaka Inamura, DDS^*, Naochika Domae, MD, PhD, Junichiro Kotani, DDS, PhD^*, and Vincent M. Figueredo, MD

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 K_ATP 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 K_ATP 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 K_ATP channels, and possibly by altered modulation of NOS expression.

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999