七氟醚预处理对肝脏缺血/再灌注损伤的保护作用

目的探讨七氟醚预处理对肝脏缺血/再灌注损伤的保护作用及其机制。方法择期全麻下行右肝癌切除术患者40例,ASA I或II级,术中经第一肝门阻断,血流阻断时间10~30 min。随机分为对照组（C组）和七氟醚预处理组（S组）。S组麻醉诱导后吸入1.0最低肺泡有效浓度七氟醚,30 min后洗脱15 min;C组不用任何吸入性麻醉药。于麻醉诱导前、肝门阻断即刻、肝门开放即刻、缺血/再灌注1 h、6 h、24 h测两组血清中ALT、AST、LDH、TNF-α、IL-1的含量,并行肝组织病理学观察。结果与麻醉诱导前比较,两组患者于肝门开放即刻、缺血/再灌注后1 h、6 h、24 h血清ALT、AST、LDH、TNF-α、IL-1浓度均显著增加（P〈0.05）;与C组比较,S组于肝门开放即刻、缺血/再灌注后相应各时点血清ALT、AST、LDH、TNF-α、IL-1浓度均降低（P〈0.05）;肝组织病理学损伤减轻。结论七氟醚预处理对肝脏缺血/再灌注损伤有保护作用,与其抑制炎症反应,减少炎性因子生成有关。

Protective effects of sevoflurane Preconditioning on hepatic ischemia reperfusion injury

Objective To investigate the protection and mechanism of sevoflurane pre-inhalation on hepatic ischemia reperfusion injury.Methods Forty ASA I or II patients under general anesthesia for right liver cancer operation in the technique blocks after the first liver gate,hepatic inflow occlusion time 10～30min,were allocated randomly into 2 group(n=20): control group(group C),sevoflurane pre-inhalation group(group S).During maintenance of anesthesia,BIS value was maintained at 40-50 in both groups.In group S patients inhaled 1.0 MAC sevoflurane for 30 min followed by 15 min of wash-out after induction of anestheia.In group C patients without any inhaled anesthetics.Serum levels of alanine aminotransferase(ALT),aspartate aminotransferase(AST),lactate dehydrogenase(LDH) TNF-α and IL-1 were determined before induction of anestheia,Pringle immediately,hepatic portal,opening up instantly,ischemia/reperfusion 1 h,6 h,24 h after ischemia-reperfusion.Results With the induction of anesthesia comparison,the two groups in the hepatic portal open instantly,ischemia / reperfusion after 1 h,6 h,24 h of serum ALT,AST,LDH,TNF-α,IL-1 levels were significantly increased(P<0.05);compared with the C group,and S group in the hepatic portal open instantly,ischemia/reperfusion the corresponding time points of serum ALT,AST,LDH,TNF-α,IL-1 levels were lower(P<0.05);pathology injury of hepatic tissue in the S group reduced.Conclusion Sevoflurane pre-inhalation can protect right liver operation from ischemia reperfusion injury.The protective mechanisms maybe related to reduceing inflammatory response and inhibition to reduce the generation of inflammatory factors.