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<0.05 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.
A case of coronary artery spasm that occurred during inadequate anesthesia, as indicated by the bispectral index(BIS) is described. A 73-year-old man with a history of variant angina was scheduled for left upper lobectomy because of lung cancer. Surgery was to be performed under general anesthesia combined with thoracic epidural anesthesia. Preoperative examination showed only complete right bundle branch block on the electrocardiogram(ECG). Anesthesia induction and intubation were uneventful. Anesthesia was maintained with nitrous oxide in oxygen, propofol and epidural block. The patient's systolic arterial pressure decreased sud-denly to about 70mmHg upon surgical manipulation of the heart, but there was no remarkable ST-T change on the ECG. The administration of propofol was terminated, and 5mg of ephedrine was injected with 100% oxygen. The BIS rose from 40 to 70. After normal systemic pressure was achieved, the ECG showed ST segment elevation. Isosorbide and nicorandil were administered, and the ST segment returned to normal. It is possible that the inadequate anesthesia, the administration of ephedrine, or both were the cause of the coronary artery spasm in this case. We should be aware of the possibility of coronary artery spasm under these conditions.