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目的:探讨前列腺素(prostaglandin,PG)缺乏条件下促胃动力药胃复安对大鼠胃黏膜的损伤作用与可能机制。 方法:PG缺乏状态由5mg/kg吲哚美辛诱导;(?)SD大鼠随机分组:对照组;胃复安两组(30mg/kg,60mg/kg);吲哚美辛两组(5mg/kg,25mg/kg);吲哚美辛5mg/kg合用胃复安三组(10mg/kg,30mg/kg,60mg/kg);阿托品组(阿托品+吲哚美辛5mg/kg+胃复安60mg/kg)。禁食24h后,生理盐水或吲哚美半灌胃,30min后皮下注射胃复安或生理盐水,阿托品灌胃前10min皮下注射,4h后取血,处死大鼠取胃行损伤测定;放免法测血浆内皮素(endothelin,ET-1);生化法测一氧化氮(nitric oxide,NO)、丙二醛(malondialdhyde,MDA)、谷胱甘肽过氧化酶(glutathione peroxi-dase,CSH-Px)含量。 结果:吲哚美半合用胃复安三组胃黏膜均有明显损伤,ET-1、MDA升高(P<0.05,P<0.01),NO、CSH-Px下降(P<0.05,P<0.01);吲哚美辛25mg/kg组损伤严重,ET-1、MDA升高(P<0.01),NO、CSH-Px下降(P<0.01,P<0.05);胃复安60mg/kg胃有轻微损伤,各指标无显著变化;其余各组未见明显损伤及指标变化。 结论:(1)PG缺乏条件下促胃动力药胃复安可引起胃黏膜出血性损伤,可能与ET-1升高、NO下降致胃黏膜微循环紊乱有关。MDA升高,GSH-Px减少可能为损伤后的继发反应结果,加剧了黏膜损伤。(2)胃?
Objective: To investigate the possible mechanism of gastric mucosal lesion in rats induced by prostaglandin (PG) in the absence of prostaglandin (PG). Methods: PG deficiency was induced by 5 mg / kg indomethacin; (?) SD rats were randomly divided into control group, metoclopramide group (30mg / kg, 60mg / kg) / a, 25mg / kg); indomethacin 5mg / kg combined with metoclopramide three groups (10mg / kg, 30mg / kg, 60mg / kg); atropine group (atropine + indomethacin 5mg / kg + 60 mg / kg). After 24-hour fasting, saline or indomethamine was given gavage 30 minutes later, subcutaneous injection of metoclopramide or normal saline, subcutaneous injection of atropine 10min before gavage, 4h after the blood was taken, The levels of endothelin (ET-1), nitric oxide (NO), malondialdehyde (MDA) and glutathione peroxidase (CSH-Px) )content. Results: Indomethacin and metoclopramide significantly decreased the levels of NO and CSH-Px in gastric mucosa (P <0.05, P <0.01, P <0.01, P <0.01) (P <0.01, P <0.05); Indomethacin 25mg / kg group had severe injury, ET-1 and MDA increased (P <0.01), NO and CSH-Px decreased Slight injury, no significant changes in each index; the other groups showed no significant damage and changes in indicators. Conclusion: (1) Gastric drug can not cause hemorrhagic gastric mucosal injury under the condition of PG deficiency, which may be related to the increase of ET-1 and the disturbance of gastric mucosal microcirculation caused by the decrease of NO. MDA increased, GSH-Px reduction may be secondary to post-injury results, exacerbating mucosal injury. (2) Stomach?