出版社：Japan Society of Circulation Control in Medicine
摘要：The present study aimed to compare the cardioprotective potencies of sevoflurane and ischemic preconditioning(IP) in vivo rabbit hearts. All anesthetized open-chest rabbits underwent 30min of left anterior descending coronary artery(LAD) occlusion followed by 3h of reperfusion. Before this, rabbits were randomized into one of six groups. Control rabbits received no intervention for 45min before LAD occlusion and reperfusion(control; n=5). The ischemia-preconditioned(IP) rabbits underwent 5min LAD occlusion followed by 10min of reperfusion(IP; n=5). In the sevoflurane(S) group, 30min of sevoflurane exposure at a 1.5% end-tidal concentration was followed by 15min of washout(S, n=5). The selective mitochondorial KATP channel blocker, 5-hydroxy-decanoate(5-HD, 5mg/kg) was given intravenously 10min before ischemic preconditioning and sevoflurane exposure, respectively, (5-HD+IP; n=5, 5-HD+S; n=5). In the sevoflurane-plus-IP group, rabbits received 30min of sevoflurane exposure at a 1.5% end-tidal concentration followed by 15min of washout before 5min LAD occlusion and 10min of reperfusion (S+IP; n = 5). At the end of the 3-h reperfusion period, area at risk and infarct size were measured. There were no differences in systemic hemodynamics among 6 groups. The area at risk showed no significant differences during baseline conditions among experimental groups. Mean infarct size was 67.4±1.5%(mean±SD) of the risk area in untreated controls. The mean infarct size was significantly smaller in the IP, S, and S+IP groups: 41.2±0.9%, 49.7±4.6%, and 40.9±3.6%, respectively(P vs . control). In contrast, mean infarct size was 56.7±2.1% in the 5-HD+IP group, and 61.6±2.8% in the 5-HD+S group. Sevoflurane-induced preconditioning as well as IP exerts infarct size limiting effect through opening of mitochondrial KATP channels. Our data suggest that there is no additive effect of sevoflurane on IP induced cardioprotection.
