JOURNAL OF OSAKA DENTAL UNIVERSITY

Vol. 41 No. 2      OCTOBER - 2007

ISSN: 0475-2058      UBIC: 172

SUMMARY

Volatile anesthetics such as isoflurane and sevoflurane induce cardioprotection mimicking ischemic preconditioning. It has been reported that isoflurane-induced myocardial preconditioning is dependent on phosphatidylinositol-3-kinase (Pl 3 K)/Akt signaling which plays a central role in reperfusion injury salvage kinase cascade. It remains unclear whether this signaling cascade is involved in sevoflurane-induced preconditioning. Isolated perfused guinea pig hearts were subjected to 30min global ischemia and 120 min reperfusion (CTL). Sevoflurane-induced preconditioning was elicited by administration of sevoflurane for 10 min at one minimum alveolar concentration (1 MAC) with 10 min washout before ischemia (SEVO). Contractile recovery was monitored by left ventricular developed pressure (LVDP) and left ventricular end-diastolic pressure (LVEDP). Infarct size (IS) was determined by triphenyltetrazolium chloride (TTC) stain. Phosphorylation of Akt, a downstream target of Pl 3 K, was assessed by western blot. After ischemia-reperfusion, SEVO had higher LVDP and lower LVEDP versus CTL. Infarct size was significantly reduced in SEVO compared to CTL (44 ±8% versus 23 ±7%). Akt phosphorylation was not increased during ischemia or at 10 min after reperfusion, which is in contrast to the findings previously demonstrated in isoflurane-induced preconditioning. Other reperfusion injury salvage kinases, such as mitogen-activated protein kinase/extracellular signal-regulated kinases (MEK) and extra-cellular signal-regulated kinase (ERK), may be more important in sevoflurane-induced preconditioning. (J Osaka Dent Univ 2007; 41 : 151-159) Key words: Sevoflurane; Preconditioning, Ischemia-reperfusion injury; Akt/protein kinase B.

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