目的 探讨右美托咪啶对大鼠急性肝缺血再灌注损伤(ischemia reperfusion injury,IRI)的保护作用。方法 SD大鼠32只,随机分为对照组(S组)、缺血－再灌注组(IR组)、右美托咪啶组(Dex组)、右美托咪啶+育亨宾组(Dex+Yoh组),每组8只。IR组制备大鼠肝缺血再灌注模型。Dex组通过尾静脉以5 μg/(kg·h )的速度持续泵注右美托咪啶1 h,余同IR组。Dex+Yoh组静脉输注右美托咪啶前10 min,静脉注射育亨宾1 mg/kg,其余同Dex组。分别测定血清AST、ALT活性,肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)浓度,肝组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量,光镜观察肝组织的病理学变化。结果 与S组比较,IR组血AST、ALT、TNF-α、IL-6,肝组织MDA水平显著增加,SOD水平下降(P＜0.05);与IR组比较,Dex组血AST、ALT、TNF-α、IL-6下降(P＜0.05),肝组织SOD水平升高,MDA 水平下降(P＜0.05),Dex+Yoh组无显著变化(P>0.05);形态学上,病理损伤程度与生化指标相符合。结论 右美托咪啶能减轻肝缺血再灌注损伤,其机制可能是激活α₂肾上腺素受体,抑制氧自由基反应和炎性因子的释放。

Objective To determine the effects of dexmedetomidine on liver ischemia reperfusion injury(IRI)in rats. Methods 32 SD rats were allocated randomly into 4 groups (n=8 per group): Sham group (S), ischemia reperfusion group (IR), Dex group and Dex+Yoh group. IR group: the rats received continuous intravenous infusion of normal saline, and liver IRI was induced. Dex group: intravenous dexmedetomidine was infused continuously at 5 μg/(kg·h) for 1 h before the liver ischemia. Dex+Yoh group: yohimbine hydrochloride (1 mg/kg) was administered intravenously 10 min before dexmedetomidine. Serum AST, ALT, TNF-α, IL-6, liver superoxide dismutase (SOD) and malonylaldehyde (MDA) were detected. Liver lesions were examined histopathologically. Results Compared with group S, the serum AST, ALT, TNF-α and IL-6, liver MDA increased while SOD decreased significantly in group IR (P<0.05). Compared with group IR, the serum AST, ALT, TNF-α and IL-6, liver MDA decreased while SOD increased significantly in group Dex (P<0.05). There was no significant difference between group IR and Dex+Yoh. The pathological injury accorded with biochemistry data. Conclusions Dexmedetomidine attenuates liver IRI, partly through the inhibition of oxygen derived free radicals and depressing liberation of cytokines via the activation of the α₂-adrenoceptor.