Sarfeh I J, Tarnawski A, Maeda R, Raymont K, Mason G R, Ivey K J
Scand J Gastroenterol Suppl. 1984;92:189-94.
Clinical observations suggest that patients with portal hypertension are more prone to erosive gastritis. To test this hypothesis we investigated gastric mucosa of rats with portal hypertension (produced by staged portal vein occlusion) and sham-operated controls before and after intragastric taurocholate. Portal pressure was 36 +/- 3 cm saline in portal hypertensive rats compared with 16 +/- 2 cm in controls (P less than 0.01). Before taurocholate no macroscopic or histologic spontaneous mucosal damage was present, but portal hypertensive rats had extensive submucosal edema. Three hours after intragastric taurocholate (2 ml, 80 mM in 0.1 N HCl), macroscopic injury comprised 13.7 +/- 1.1% of mucosal surface in portal hypertensive rats compared with 3.6 +/- 0.6% in controls (P less than 0.01) confirmed also by histologic morphometry. H+ back-diffusion was 402 +/- 40 microEq/h in portal hypertensive rats and 217 +/- 30 microEq/h in controls (P less than 0.01). We conclude taurocholate induced gastric mucosal injury is enhanced by portal hypertension. Greater H+ back-diffusion in portal hypertensive rats suggests increased mucosal permeability contributed by submucosal edema. We confirm quantitatively in an experimental model that portal hypertension predisposes to gastric mucosal injury.
临床观察表明,门静脉高压患者更易患糜烂性胃炎。为验证这一假说,我们研究了门静脉高压大鼠(通过分期门静脉闭塞术制备)和假手术对照组在胃内注入牛磺胆酸盐前后的胃黏膜情况。门静脉高压大鼠的门静脉压力为36±3cm盐水柱,而对照组为16±2cm盐水柱(P<0.01)。在注入牛磺胆酸盐之前,未发现宏观或组织学上的自发性黏膜损伤,但门静脉高压大鼠有广泛的黏膜下水肿。胃内注入牛磺胆酸盐(2ml,0.1N HCl中80mM)3小时后,门静脉高压大鼠的宏观损伤占黏膜表面的13.7±1.1%,而对照组为3.6±0.6%(P<0.01),组织形态计量学也证实了这一点。门静脉高压大鼠的H+反向扩散为402±40微当量/小时,对照组为217±30微当量/小时(P<0.01)。我们得出结论,门静脉高压会增强牛磺胆酸盐诱导的胃黏膜损伤。门静脉高压大鼠中更大的H+反向扩散表明黏膜下水肿导致黏膜通透性增加。我们在一个实验模型中定量证实,门静脉高压易导致胃黏膜损伤。