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首页> 外文期刊>Life sciences >Pathogenic importance of pepsin in ischemia/reperfusion-induced gastric injury.
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Pathogenic importance of pepsin in ischemia/reperfusion-induced gastric injury.

机译：胃蛋白酶在缺血/再灌注引起的胃损伤中的致病重要性。

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We investigated the role of pepsin in the development of ischemia/reperfusion (I/R)-induced gastric lesions in rats. Under urethane anesthesia, the pylorus was ligated, the celiac artery was clamped, and 1 ml of HCl (50-150 mM) was instilled in the stomach. Then, reperfusion was established 15 min later by removing the clamp, and 2 h later the stomach was assessed for gross mucosal damage. Pepstatin (a specific pepsin inhibitor) or pepsin was given i.g. after the pylorus was ligated while cimetidine, omeprazole, or atropine was given s.c. 30 min before the ligation. I/R produced hemorrhagic gastric injury, with a concomitant increase in the amount of pepsin secreted, and the degree of both these responses was dependent on the concentration of HCl. The formation of lesions by IR in the presence of 100 mM HCl was significantly prevented by atropine or bilateral vagotomy, but neither omeprazole nor cimetidine had any effect. Intragastric administration of pepstatin dose-dependently reduced the severity ofthe I/R-induced gastric lesions, the effect being significant even at 0.1 mg/kg, while that of pepsin markedly aggravated these lesions. The increased pepsin output during I/R was associated with luminal acid loss and significantly inhibited by bilateral vagotomy or pretreatment with atropine but not cimetidine or omeprazole, while pepstatin significantly inhibited the pepsin activity. In conclusion, we suggest that pepsin plays a pivotal role in the pathogenesis of I/R-induced gastric lesions, and pepsin secretion is increased during I/R, the process being associated with acid back-diffusion and mediated through a vagal-cholinergic pathway.
机译：我们调查了胃蛋白酶在大鼠缺血/再灌注（I / R）引起的胃部病变中的作用。在尿烷麻醉下，结扎幽门，夹住腹腔动脉，并将1 ml的HCl（50-150 mM）滴入胃中。然后，在15分钟后通过移开固定夹建立再灌注，并在2小时后评估胃的粘膜总损害。给予胃抑素（一种特定的胃蛋白酶抑制剂）或胃蛋白酶。幽门结扎后给予西咪替丁，奥美拉唑或阿托品s.c.结扎前30分钟。 I / R引起出血性胃损伤，胃蛋白酶分泌量随之增加，而这两种反应的程度均取决于HCl的浓度。阿托品或双侧迷走神经切断术可在100 mM HCl存在下通过IR形成病变，但奥美拉唑和西咪替丁均无任何作用。胃内施用胃蛋白酶抑制素可剂量依赖性地降低I / R诱导的胃部病变的严重程度，即使在0.1 mg / kg时，这种作用也很明显，而胃蛋白酶则明显加重了这些病变。 I / R期间胃蛋白酶输出的增加与管腔酸的丢失有关，并被双侧迷走神经切断术或阿托品预处理明显抑制，而西咪替丁或奥美拉唑则无明显抑制作用，而胃抑素则明显抑制胃蛋白酶活性。总之，我们认为胃蛋白酶在I / R诱导的胃部病变的发病机理中起着关键作用，胃蛋白酶的分泌在I / R期间增加，该过程与酸的反向扩散有关，并通过迷走胆碱能途径介导。

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