门静脉高压性脾动脉病变

Portal hypertensive vasculopathy of splenic artery

目的探讨肝硬化患者脾动脉壁的病理变化。方法以光镜、电镜、免疫组化法观察２１例肝硬化患者和１５例正常人脾动脉壁的病理变化和诱导型一氧化氮合酶（ｉｎｄｕｃｉｂｌｅｎｉｔｒｉｃｏｘｉｄｅｓｙｎｔｈａｓｅ，ｉＮＯＳ）的表达。结果与正常人对比，肝硬化患者脾动脉内膜增厚，内皮细胞不完整，内弹性膜变平并分裂和断裂，中膜平滑肌增厚，并迁移至内膜下，电镜下见平滑肌细胞变性、萎缩，有的肥大、增生和表型由收缩型向合成型转化。ｉＮＯＳ表达增强。管壁细胞外基质增多，致管壁胶原化和纤维化。结论肝硬化患者脾动脉可继发病理变化，使其收缩结构破坏和ｉＮＯＳ活性增强，这是导致血管对缩血管活性物质反应性下降的原因之一。

Objective To study the pathological changes of splenic artery wall in portal hypertensive patients.HZMethods The pathological changes and iNOS activity of splenic artery wall were studied in 21 patients with liver cirrhosis and 15 normal sabiects, using light and electron microscope and immunohistochemistry.5HZResults Compared with normal individuals,the splenic artery of cirrhotic patients showed that the intima was thickened,split and broken, and the smooth muscle layer of middle membrane was thicker and migrated to underintima space. In cirrhotic patients, regression,atrophy or hypertrophy and hyperplasia were seen in smooth muscle cells whose contractile phenotype changed to synthetic phenotype as well. iNOS activated obviously. Extracellular matrix increased in the wall,resulting in collagenic and fiberous changes.5HZConclusions Hemodynamic alteration due to liver cirrhosis induced pathological changes of splenic artery,including the damage to contractile structure and increase of iNOS activity.It is one of the reasons of decrease of artery reaction to contractile vasoactive materials.