应激状态下胃粘膜组织内皮素-1水平及其免疫组化研究

为探讨内皮素（ET）－1在应激性溃疡（SU）发病中的意义，以大鼠冷束缚应激溃疡（CRS）为模型，采用免疫组化及放免方法，观察研究应激前后大鼠胃粘膜组织ET－1表达分布、含量及胃粘膜损伤溃疡指数（UI）等变化情况。结果显示，ET－1阳性表达物质主要分布于胃粘膜血管内皮细胞、胃粘膜上皮细胞、粘膜肌层平滑肌细胞的胞浆，应激3h后胃粘膜组织ET－1阳性表达细胞数量与强度均较正常对照组明显增加（P＜0．05）。放免显示应激1h后胃粘膜组织ET－1含量即较正常对照组明显升高（P＜0．01），且在应激后12h内呈持续升高状态，同时随着ET－1的升高，UI不断增加，两者呈显著正相关（r＝0．98，P＜0．01）。提示在冷束缚应激诱导大鼠SU形成过程中，胃粘膜组织局部可大量增加ET－1的合成、分泌，从而参与SU的病理生理过程，可能是胃粘膜损伤的重要致病因子。

IMMUNOHISTOCHEMISTRY STUDY AND LEVELS OF ENDOTHELIN-1 IN GASTRIC MUCOSA OF COLD-RESTRAINT-STRESS RATS

To investigate the role of ET 1 in the pathogenesis of SU, a model was established by cold restraint stress(CRS) inducing rat ulcer, immunohistochemistry(IHC)ABC method and radioimmunoassay(RIA) methods were used to determine ET 1 content and to study the expression and location of ET 1 in stomach of normal and CRS rats,and to evaluate the ulcer index(UI). IHC showed that ET 1 was stained as brownish grains,localized in the cytoplasm of vascular endothelial cells, stomach smooth muscle cells, gastric epithelial and vascular smooth muscule cells around lamina muscularis mucosae in stomach. The proportion of ET 1 positive cells was significantly higher in 3h poststress gastric mucosa than in normal gastric mucosa in rats by IHC( P <0 05);RIA showed that ET 1 level in gastric mucosa increased significantly 1h poststress compared with the control values( P <0 01),and ET 1 level in gastric mucosa continued to increase significantly during 12 hour stress. Moreover, there was positive relationship between gastric mucosal ET 1 and UI( r =0 98, P <0 01). The results suggest that in the process of formation of SU,ET 1 may be synthesized and secreted by gastric mucosa of CRS rats,and plays an important role in the pathogenesis of SU.