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作 者:蒋群[1,2] 屠伟峰[1] 杨垂勋[1] 李成龙[3]
机构地区:[1]广州军区广州总医院全军临床麻醉中心,510010 [2]南方医科大学 [3]广东省第二中医院麻醉科,广州市510095
出 处:《实用医学杂志》2010年第11期1926-1929,共4页The Journal of Practical Medicine
摘 要:目的:观察阿米洛利(amiloride)预处理对浸水束缚应激大鼠胃黏膜损伤的影响。方法:30只雄性Wistar大鼠随机分为正常对照组(NC组,n=10)、WIRS对照组(WS组,n=10)和amiloride预处理组(AM组,n=10)。在(20±1)℃水温下,浸水束缚应激法复制大鼠急性胃黏膜病变模型。6h后处死取胃组织标本,10倍解剖显微镜下观察各组胃黏膜溃疡指数(UI),光学显微镜下观察各组标本组织学改变,并用比色法测定各组胃组织中丙二醛(MDA)与超氧化物歧化酶(SOD)的含量变化。结果:WS组大鼠胃黏膜呈暗红色,有大量点状出血、线状出血或片状糜烂,黏膜下血管和皮区血管充血,光镜下上皮细胞黏液层变薄、缺失,细胞间隙变大,有不同程度的坏死;而AM组大鼠浸水束缚应激6h后大鼠黏膜出血或糜烂程度较WS组明显好转,光镜下虽可见大量毛细血管充血扩张,上皮细胞黏液层有少许缺损,但基本完整。与NC组比较,WS组大鼠浸水束缚应激6h后,胃黏膜UI显著增高(P<0.01),胃组织SOD活性降低,MDA含量显著增高(P<0.01);Amiloride预处理能显著降低浸水束缚应激大鼠UI(P<0.01),提高SOD活性,降低MDA水平(P<0.01)。结论:Amiloride可有效地保护氧自由基介导性浸水束缚应激大鼠急性胃黏膜损伤或病变,提示酸敏感离子通道可能参与了浸水束缚应激大鼠急性胃黏膜病变的发生机制。Objective To observe the effect of amiloride pretreatment on acute gastric mucosal lesion(AGML) induced by water immersion and restraint stress(WRIS) in rats.Methods Thirty Wistar rat were randomly divided to 3 groups(10 animals per group), including normal control group(Group NC), WRIS group(Group WS), amiloride preconditioning group(Group AM).Gsatric mucosal lesion model was induced by WRIS in water temperature(20 ± 1)℃.After 6 h of WRIS, gastric tissues were excised and gastric ulcer index was observed and countered in the 10 anatomical microscope, the levels of MDA and SOD in gastric tissues were determinated by colorimetric assay.Results After 6 h of WIRS, the gastric mucosal was severely injured, the gastric level of MDA was significantly increased likewise UI, while the level of SOD was decreased significantly.Amiloride could attenuates significantly gastric lesion degrees(P 0.01).Compared with Group WS, the gastric level of SOD was increased significantly in Group AM, while the concentration of MDA was decreased remarkedly.Conclusion Amiloride can enhance the resistance of gastric mucosal to injury by scavenging the reactive oxygen species, so ASICs may participate in the development of AGML induced by WIRS.
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