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目的 探讨门静脉高压性胃病(PHG)的发病机理。方法 设计2组门静脉高压症动物模型,并与假手术组对照观察胃粘膜组织形态以及超微结构的病理变化,并通过微机图像处理系统对组织学图像进行定量分析。结果 门静脉高压时胃粘膜水肿明显,散在分布红点和/或瘀斑。光镜及扫描电镜检查均发现上皮细胞肿胀、崩解或脱落,腺体数目减少,粘膜变薄,无炎性细胞浸润和上皮细胞化生;粘膜下层水肿增厚。粘膜微血管结构的改变最具特征性。光镜见粘膜层毛细血管以及粘膜基底层和粘膜下层微静脉明显扩张。透射电镜则显示毛细血管变形,腔狭窄,细胞连接松散;内皮细胞内有大量的吞饮小泡;微静脉中膜内的平滑肌细胞、胶原纤维等细胞外基质增生。定量分析示门静脉高压大鼠微血管形态的改变表现为胃壁相对血管腔面积和相对血管壁面积显著高于假手术组;门静脉高压大鼠胃粘膜的损伤比与门静脉压力呈正相关,且肝硬化组明显大于门静脉狭窄组。结论 肝硬化门静脉高压症时伴有独特的胃部微血管形态学的异常,这种异常是PHG发生的病理学基础,是门静脉高压症病理变化的一部分。
Objective To investigate the pathogenesis of portal hypertensive gastropathy (PHG). Methods Two groups of models of portal hypertension were established. The morphology of gastric mucosa and pathological changes of the ultrastructure were observed with the sham-operation group. The histological images were quantitatively analyzed by computerized image processing system. Results Gastric mucosal edema was obvious when portal hypertension occurred, scattered red spots and / or ecchymosis. Light microscopy and scanning electron microscopy showed epithelial cell swelling, disintegration or shedding, the number of glands decreased, mucosal thinning, no inflammatory cell infiltration and epithelial metaplasia; submucosal edema thickening. Mucous microvascular changes in the most characteristic structure. Light microscopy of mucosal capillary and mucosal basal and submucosal venules significantly dilated. Transmission electron microscopy showed capillary deformation, narrow lumen, loosely connected cells; a large number of swallowed vesicles in endothelial cells; smooth muscle cells, collagen fibers and other extracellular matrix hyperplasia in the venules of the venules. Quantitative analysis showed that the morphological changes of microvessels in portal hypertension rats showed that the relative cavity area and relative vessel wall area in gastric wall were significantly higher than those in sham operation group. The gastric mucosal injury in portal hypertension rats was more positively correlated with portal vein pressure than in sham operation group Greater than the portal vein stenosis group. Conclusions Liver cirrhosis with portal hypertension accompanied by a unique abnormal morphology of gastric microvessels, this abnormality is the pathological basis of PHG occurs, is part of the pathological changes of portal hypertension.