山莨菪碱对肝脏缺血再灌注损伤的保护作用

The protective mechanism of anisodamine on liver ischemia-reperfusion injury in rats

目的 探讨山莨菪碱对肝脏缺血再灌注损伤的保护作用。方法 将雄性Wistar大鼠制成肝脏缺血再灌注模型 ,随机分为正常对照组、缺血再灌注组、生理盐水组和山莨菪碱组 ,观察肝脏缺血 6 0min再灌注 1、3、6、12及 2 4h后血浆和 /或肝组织中内皮素 1(ET 1)、透明质酸 (HA)、丙氨酸转氨酶 (ALT)、丙二醛 (MDA)和再灌注 1h后肝细胞内游离Ca2 + ([Ca2 + ]i)、ATP含量变化以及肝组织病理学改变。结果 肝脏缺血再灌注后血浆和 /或肝组织中ET 1、HA、ALT、MDA和肝细胞内[Ca2 + ]i 含量均显著升高 ,而肝组织中ATP含量明显降低 ;肝脏缺血再灌注前应用山莨菪碱 2 .0mg/kg者 ,血浆HA和肝细胞内 [Ca2 + ]i含量明显降低 ,肝组织中MDA也有不同程度的降低 ,而肝组织中ATP含量明显升高 ,同时肝酶的漏出减少 ,肝组织病理学损害明显减轻。

Objective To study the protective mechanism of anisodamine on liver ischemia-reperfusion injury in rats.Methods One hundreds and sixty male Wistar rats were randomly divided into the normal control group (n=10), ischemia-reperfusion group (n=50), physiologic saline group (n=50)and anisodamine group (n=50). The animals were killed at 1st,3rd, 6th,12th,24th h after ischemia induced for 60 min and followed by reperfusion. Plasma and(or) liver endothelin-1 (ET-1), hyaluronic acid (HA), glutamic-pyruvic transaminase enzyme (ALT) and malondialdehyde (MDA) were measured. Liver intracellular i and adenosine triphosphate (ATP) after being reperfused for 1 h were measured. Meanwhile, the histopathologic hepatic alterations were also observed.Results Plasma ET-1, HA, ALT and liver ET-1, MDA, intracellular i concentrations were markedly increased and liver ATP markedly decreased after liver ischemia-reperfusion. It was found that an intravenous injection of anisodamine (2.0 mg/kg) before ischemia-reperfusion could significantly decrease the levels of HA, ALT, MDA, intracellular i and increase ATP concentrations in plasma and(or) liver. Meanwhile, the histopathologic hepatic alterations were significantly lessened.Conclusions The anisodamine have protective effects on liver ischemia-reperfusion injury.