盐酸戊乙奎醚对失血性休克大鼠肠黏膜的保护作用

目的拟用失血性休克模型来研究盐酸戊乙奎醚是否对肠黏膜缺血再灌注损伤具有保护作用。方法将雄性SD大鼠随机分为四组(n=8):对照组、休克组、小剂量盐酸戊乙奎醚组(0.15 mg/kg)和大剂量盐酸戊乙奎醚组(0.30mg/kg)。盐酸戊乙奎醚或等量生理盐水在休克前30 min通过尾静脉注入大鼠体内。除对照组外,其他三组经15 min股动脉缓慢放血使大鼠平均动脉压达(40±5)mm Hg(1 mm Hg=0.133 kPa)诱发失血性休克,通过放血或输血维持大鼠休克状态60 min。休克结束30 min内输注大鼠自身血液和林格液(32 mL/kg)进行复苏。复苏4 h之后检测肠黏膜pH(pHi)、一氧化氮(NO)、超氧化物歧化酶(SOD)、丙戊二醛(MDA)及钙离子(Ca2+)的含量,并观察肠黏膜组织病理学改变。结果与休克组比较,大剂量盐酸戊乙奎醚组NO、MDA及Ca2+的含量显著降低;而SOD活性和pHi增高。与此相应的是肠黏膜细胞凋亡及组织病理学评分降低。结论大剂量盐酸戊乙奎醚对失血性休克大鼠肠黏膜具有保护作用,其机制可能与抑制细胞死亡和保存细胞抗氧化功能相关。

Penehyclidine hydrochloride preconditioning protect against intestinal mucosa injury in hemorrhagic shock rats

Objective To study the effects and the mechanism of Penehyclidine hydrochloride（PHC） on intestinal mucosa injury caused by ischemia reperfusion（IR）.Methods Male sprague-dawley（SD） rats were randomly divided into four groups： the control group,the hemorrhagic shock group,the 0.15 mg/kg PHC group,and the 0.30 mg/kg PHC group（n = 8）.Saline or PHC were administered before hemorrhagic shock for thirty minutes.In addition to the control group,mean arterial pressure of the other three groups for rats by 15 min femoral artery slow blood was reached（40±5） mm Hg（1 mm Hg = 0.133 kPa） to induce uncontrolled hemorrhagic shock,through the depletion or blood transfusion maintain to keep rats shock state for 60 min.After shock over 30 min in rats,they were given own blood infusion and ringer＇s liquid（32 mL/kg） for recovery.Four hours after resuscitation Ca2＋,NO and the pH in intestinal mucosa,and the intestinal mucosa histopathology were measured.The malondialdehyde（MDA） and superoxide dismutase（SOD） in the intestinal mucosa were also tested.And intestinal mucosal pathology change was observed.Results Large doses PHC enhanced pH and decreased NO,MDA and Ca2＋ in intestinal mucosa and increased SOD activity and pHi,compared with the hemorrhagic shock group,and the intestinal mucosal apoptosis,and the histological score decreased.Conclusion Large doses PHC preconditioning provides an effective protection against intestinal mucosa injury in hemorrhagic shock.The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation in intestinal mucosa.