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作 者:张文文[1] 张建福[1] 徐明[2] 张咏梅[1]
机构地区:[1]徐州医学院神经生物学研究中心 [2]徐州医学院病理生理学教研室,江苏徐州221002
出 处:《徐州医学院学报》2007年第3期141-144,共4页Acta Academiae Medicinae Xuzhou
基 金:国家自然科学基金(30370533;30570671);江苏省教育厅科学研究基金(05KJB310134)
摘 要:目的观察腹腔注射催产素(oxytocin,OT)对胃缺血-再灌注损伤(gastric ischemia-reperfusion injury,GI-RI)的作用及其可能的机制。方法采用夹闭大鼠腹腔动脉30min,松开动脉夹血流复灌1h,制备胃缺血-再灌注损伤模型;将SD大鼠随机分为12组,每组6只;4组腹腔注射0.5ml生理盐水和0.5ml4,20,100μg/0.5ml剂量的OT;1组腹腔注射200μg/0.5ml阿托西班(atosiban,OT特异性阻断剂),1组等剂量atosiban注射10min后给予100μg/0.5mlOT;另取4组分别进行迷走神经切除、交感神经切除以及迷走神经切断+100μg/0.5mlOT腹腔注射和交感神经切除+100μg/0.5mlOT腹腔注射;这10组均进行缺血再灌注,计数胃黏膜损伤指数(gastric mucosal damage index,GMDI)。剩余2组分别给予0.5ml生理盐水和100μg/0.5mlOT,采用幽门结扎法收集胃液,测定所得胃液体积和pH值。结果与对照组相比,腹腔注射OT(20,100μg/0.5ml)后,GI-RI明显减轻,GMDI减少,并能减少胃液排出量和胃酸度(P<0.05);特异性拮抗剂atosiban能够翻转OT的保护作用;切断膈下迷走神经或切除腹腔交感神经节后再给予OT,可进一步减轻GI-RI。结论腹腔注射OT对大鼠GI-RI具有保护作用;这种作用可能是由迷走和交感神经介导,通过OT受体发挥的。Objective To investigate the effect of peripherally administered oxytocin (OT) on gastric ischemia-reperfusion injury (GI-RI) and its possible mechanism. Methods The animal GI-RI models were established on SD rats by clamping the celiac artery for 30 min to induce ischemia and allowing reperfusion for 1 h. The SD rats were randomly divided into 12 groups (n=6 each). Four of them were given ip NS 0.5 ml and OT 4 μg, 20 μg and 100 μg in 0.5 ml of NS ; one group was given atosiban 200 μg / 0.5 ml (a selective OT receptor antagonist); one group was given OT 100 μg / 0.5 10 min after atosiban; four groups were subjected to the operations of vagotomy, sympathectomy, vagotomy plus OT and sympathectomy plus OT. GI-R was then induced in all of the ten groups, and the extents of GI-RI were assessed by scoring the gastric mucosal damage index (GMDI). Lastly, the other two groups were given NS 0.5 ml and OT 100 μg / 0.5 ml respectively, and then the method of pylorus ligation was used to collect the gastric juice to determine its volume and pH. Results Compared with the control group, it was found that the GI-RI was obviously attenuated (P<0.05) after intraperitoneal administration of OT (20 μg and 100 μg / 0.5 ml), the gastric juice output and acidity were also reduced (P<0.01). The protective effects of OT could be reversed by atosiban; and OT could further attenuate the GI-RI after vagotomy or sympathectomy (P<0.01). Conclusion OT could significantly protect gastric mucosal against injury induced by ischemia-reperfusion. This effect may be mediated through the vagus and sympathetic nerve, with the OT receptors involved.
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