Sarfeh I J, Tarnawski A, Hajduczek A, Stachura J, Bui H X, Krause W J
Department of Surgery, Long Beach Veterans Administration Medical Center, Irvine, Calif.
Surgery. 1988 Jul;104(1):79-85.
We assessed macroscopic, histologic, ultrastructural, and functional features of aspirin-induced gastric mucosal injury in portal hypertensive and sham-operated rats. Portal hypertension was produced by staged portal vein ligation. Four hours after intragastric acidified aspirin administration, intraluminal pH in portal hypertensive rats was 6.6 +/- 0.2 and 4.3 +/- 0.5 in sham-operated controls (p less than 0.01). Gross mucosal damage was significantly greater in portal hypertensive rats compared with controls (18 +/- 2 versus 7 +/- 1% of total mucosal area). Histologic deep necrosis involved 22 +/- 2% of mucosal section lengths in portal hypertensive rats compared with 7 +/- 1% in sham-operated rats (p less than 0.01). In portal hypertensive rats, histologic and ultrastructural evaluation demonstrated capillary endothelial abnormalities, arterialization of submucosal veins, and markedly greater severity of microvascular damage than in sham-operated controls. Neutralized aspirin (pH, 7.0) did not produce any significant damage detectable grossly, histologically, or by transmission electron microscopy in portal hypertensive rats. We conclude that acid-dependent aspirin-induced gastric mucosal damage is significantly increased in portal hypertension.
我们评估了门静脉高压大鼠和假手术大鼠阿司匹林诱导的胃黏膜损伤的宏观、组织学、超微结构及功能特征。门静脉高压通过分期门静脉结扎产生。胃内给予酸化阿司匹林4小时后，门静脉高压大鼠的管腔内pH值为6.6±0.2，假手术对照组为4.3±0.5（p<0.01）。与对照组相比，门静脉高压大鼠的大体黏膜损伤明显更严重（分别占总黏膜面积的18±2%和7±1%）。组织学上，门静脉高压大鼠黏膜切片深度坏死占22±2%，假手术大鼠为7±1%（p<0.01）。在门静脉高压大鼠中，组织学和超微结构评估显示毛细血管内皮异常、黏膜下静脉动脉化，且微血管损伤的严重程度明显高于假手术对照组。在门静脉高压大鼠中，中和后的阿司匹林（pH值为7.0）在大体、组织学或透射电子显微镜下均未产生任何明显的损伤。我们得出结论，在门静脉高压状态下，酸依赖性阿司匹林诱导的胃黏膜损伤显著增加。
