Sarfeh I J, Tarnawski A, Malki A, Mason G R, Mach T, Ivey K J
Gastroenterology. 1983 May;84(5 Pt 1):987-93.
The present study was performed primarily in order to determine whether gastric mucosa of rats with portal hypertension has different functional and histologic features when compared with controls, and second to quantitate and compare morphologic and functional changes after exposure to topical ethanol. Portal hypertension was produced by staged portal venous occlusion, and in these animals portal pressure was 32 +/- 2 cm saline compared with 18 +/- 2 cm in sham-operated controls (p less than 0.005). Before ethanol, portal hypertensive rats compared with controls had significantly higher luminal pH (2.9 +/- 0.3 vs. 1.9 +/- 0.1), increased H+ back-diffusion (loss of 138 +/- 10 vs. 57 +/- 16 microEq H+/h), lower potential difference (8 +/- 1 mV lower than controls), and extensive submucosal edema (submucosal thickness 325 +/- 25 vs. 138 +/- 18 micrometers). After 3 h of exposure to 2 ml intragastric absolute ethanol, the area of macroscopic hemorrhagic mucosal injury was significantly greater in portal hypertensive rats than in controls (34.0 +/- 8.7% vs. 7.6 +/- 2.1%), confirmed histologically by the greater number of deep hemorrhagic necrotic lesions and extent of mucosal length involved. Furthermore, after ethanol, portal hypertensive rats compared with controls had significantly increased gastric volume (14.4 +/- 1.5 vs. 8.3 +/- 0.6 ml), Na+ (86.6 +/- 8.0 vs. 64.6 +/- 8.0 mEq/L), pH (7.1 +/- 0.3 vs. 4.3 +/- 0.4), H+ back-diffusion (loss of 309 +/- 41 vs. 207 +/- 33 microEq H+/h), and protein and blood loss (100% increases over controls). These results indicate that gastric mucosa of portal hypertensive rats has distinctive functional and histologic abnormalities that can explain its increased susceptibility to erosive injury after ethanol. This study quantitatively confirms in an animal model the clinical observations that portal hypertension may predispose to severe gastric mucosal injury.
本研究主要是为了确定门静脉高压大鼠的胃黏膜与对照组相比是否具有不同的功能和组织学特征，其次是定量并比较局部应用乙醇后形态学和功能的变化。通过分期门静脉阻塞来制造门静脉高压，这些动物的门静脉压力为32±2cm盐水柱，而假手术对照组为18±2cm盐水柱（p<0.005）。在给予乙醇之前，门静脉高压大鼠与对照组相比，管腔内pH值显著更高（2.9±0.3对1.9±0.1），H+反向扩散增加（损失138±10对57±16微当量H+/小时），电位差更低（比对照组低8±1mV），并且有广泛的黏膜下水肿（黏膜下厚度325±25对138±18微米）。在给予2ml胃内无水乙醇3小时后，门静脉高压大鼠的宏观出血性黏膜损伤面积显著大于对照组（34.0±8.7%对7.6±2.1%），组织学上表现为深部出血性坏死病变数量更多以及涉及的黏膜长度范围更广。此外，给予乙醇后，门静脉高压大鼠与对照组相比，胃容积显著增加（14.4±1.5对8.3±0.6ml），Na+（86.6±8.0对64.6±8.0毫当量/升），pH（7.1±0.3对4.3±0.4），H+反向扩散（损失309±41对207±33微当量H+/小时），以及蛋白质和血液损失（比对照组增加100%）。这些结果表明门静脉高压大鼠的胃黏膜具有独特的功能和组织学异常，这可以解释其在乙醇作用后对糜烂性损伤易感性增加的原因。本研究在动物模型中定量证实了门静脉高压可能易导致严重胃黏膜损伤的临床观察结果。
