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Abstract
Objective To investigate the role of the mitochondrial ATP-sensitive potassium (mito-K_(ATP)) channel in sevoflurane preconditioning-reduced focal cerebral ischemia-reperfnsion (I/R) injury in rats. Methods One hundred healthy 3-4 month old male SD rats 250-300 g were randomly assigned into 5 groups (n = 20 each) : group Ⅰ sham operatiun (group S); group Ⅱ I/R; group Ⅲ sevoflurane preconditioning (group Sevo); group Ⅳ 5-hydroxydecannate (5-HD) and group Ⅴ 5-HD + Sevo. Focal cerebral I/R was produced by mid-cerebral artery occlusion (MCAO) in group Ⅱ-Ⅴ . Cerebral ischemia was maintained for 2 h followed by 6 and 24 h reporfnsiun. In group Ⅲ and Ⅴ 2.4% sevoflurane in 97.6% O_2 was inhaled for 60 min at 24 h before MCAO. In group Ⅴ 5-HD (a selective mito-K_(ATP) channel antagonist) 40 mg/kg was given intraporitoneally (IP) at 30 min before sevoflurane preconditioning. In group Ⅳ 100% O_2 was inhaled instead of sevoflurune and 5-HD 40 mg/kg was given IP at 30 min before O_2 inhalation. Neurological deficit score (NDS, 0=no deficit, 7 = death) were measured at 6 and 24 h of reperfusion and the animals were then killed. Their brains were removed for determination of infaret size by TTC and cellular translocation of PKCe by Western blot analysis. Results NDS were significantly lower and brain infarct size was significantly smaller in group.Sevo (Ⅲ) than in I/R group (Ⅱ). The neuroprotection induced by sevoflurane preconditioning was reversed by 5-HD 40 mg/kg in group Ⅴ (5-HD + Sevo). There was no significant difference in infarct size and NDS among group Ⅱ , Ⅳ and Ⅴ . PKCe was activated and translocated to the membrane fraction at 6 h of reperfusion in group Sevo (Ⅲ) and this effect of sevoflurane was also abolished by 5-HD in group Ⅴ (5-HD + Sevo). Conclusion Scvoflurane preconditioning-induced neuroprotection is mediated by mito-K_(ATP) channel probably through regulating PKCe membrane translocation. Key words: Anesthetics,inhalation; Ischemic preconditioning; KATP channels; Brain; Reperfusion injury
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