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作 者:赵永忠[1] 王波[1] 王天才[1] 梁扩寰[1] 李德明[1]
机构地区:[1]华中科技大学同济医学院附属同济医院肝病研究所,武汉430030
出 处:《华中科技大学学报(医学版)》2003年第2期163-165,170,共4页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基 金:卫生部计财司临床重点学科建设基金资助项目(No. 0 7-95 0 10 - 2 )
摘 要:目的 探讨血管内皮生长因子在大鼠门脉高压性胃病发病机制中的作用。方法 SD大鼠随机分为门静脉高压 (portal hypertensive,PHT)组和假手术 (sham- operated,SO)组。采用门静脉主干部分结扎复制门脉高压模型 ,于术后第 14 d,测量门静脉压力、胃底及胃窦黏膜血流量 ;采用免疫组织化学 SABC法检测胃组织血管内皮生长因子 (vas-cular endothelial growth factor,VEGF)表达情况。结果 PHT组大鼠门静脉压力 [(19.89± 2 .2 9) mm Hg]和胃底黏膜血流量 [(116 .2 1± 13.4 0 ) BPU]显著高于 SO组 [(8.5 3± 0 .84 ) mm Hg,(79.0 1± 11.6 6 ) BPU](P<0 .0 1,P<0 .0 5 )。而胃窦黏膜血流量在 PHT组和 SO组之间无显著性差异 (P>0 .0 5 )。免疫组化发现血管内皮生长因子在 PHT组大鼠胃黏膜组织中呈强阳性表达 ,在 SO组则呈弱阳性表达。结论 VEGF可能参与了门脉高压性胃病 (portal hyper-tensive gastropathy,PHG)的发病机制 ,门脉高压性胃病所致的上消化道出血可能与Objective To investigate the role of vascular endothelial growth factor (VEGF) in the pathogenesis of portal hypertensive gastropathy (PHG) in rats. Methods Sprague Dawley rats were randomly divided into two groups: portal hypertensive group(PHT)and sham operated group (SO). The portal hypertensive models were established by portal vein ligation. At 14th day after operation, the portal vein pressure (PVP), the gastric mucosal blood flow (GMBF) in antrum and fundus were measured; the expression of VEGF in gastric mucosal specimens was detected by means of SABC. Results The PVP (19 89±2 29 mmHg) and GMBF (116 21±13 40 BPU)in fundus were significantly higher in the portal hypertensive group than in the sham operated group (8 53±0 84 mmHg, 79 01±11 66 BPU, respectively)( P <0 01 or P <0 05 respectively). The GMBF in antrum showed no significant difference between the PHT group and the SO group ( P >0 05). The expression level of VEGF in the gastric mucosa of PHT group was significantly higher than in the SO group. Conclusion VEGF may participate in the pathogenesis of portal hypertensive gastropathy. The hemorrhage in the upper gut caused by portal hypertensive gastropathy may be related to VEGF.
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