门脉高压症患者内脏血管壁的组织病理学改变  

Study on the Relationship between the Portal Hypertension and Portal Hypertensive Vasculopathy

作　　者：杨镇[1] 任大宏[2] 李大鹏[1] 裘法祖[1] 

机构地区：[1]同济医科大学附属同济医院外科,武汉430030 [2]同济医科大学基础医学院病理学教研室,武汉430030

出　　处：《同济医科大学学报》2000年第1期34-36,共3页Acta Universitatis Medicinae Tongji

基　　金：国家自然科学基金!(No.39470685)

摘　　要：５０例门脉高压症患者在行脾切除贲门周围血管离断术时取脾动脉、脾静脉和胃冠状静脉行光镜和电镜观察，用免疫组织化学法分析脾动脉壁诱导型一氧化氮合酶（ｉＮＯＳ）的表达，以研究门脉高压症和门脉高压性血管病变之间的因果关系。结果表明：①脾动脉壁的内弹性膜和弹力纤维断裂和变性，平滑肌细胞萎缩、凋亡和表型改变，平滑肌细胞ｉＮＯＳ呈阳性表达，其活性较非肝硬变患者明显提高（Ｐ＜０．０１）。②胃冠状静脉和脾静脉壁内膜增生，形成新内膜，广泛的附壁血栓形成，有类粥样硬化样斑块，伴有平滑肌细胞肥大。静脉的中膜平滑肌纤维明显增粗、变厚，伴细胞外基质聚积。提示：门脉高压症时合并有内脏动脉和静脉的血管病变。门脉高压症、内脏高动力循环和内脏血管病变在门脉高压症的发病机制中具有互为因果的关系。The relationship between the portal hypertension and portal hypertensive vasculopathy was investigated. The splenic arteries, splenic veins and gastric coronary veins of portal hypertensive patients (n = 50) were obtained during pericardial devascularization and examined under optical and electron microscopy. The expression of iNOS in splenic arterial wall was analyzed using immunohistochemistry. The results showed as follows: (1) The internal elastic membrane and elastic fiber of splenic artery media were broken and degenerated. The atrophy, apoptosis and phenotype changes were found in the smooth muscle cells of splenic artery. The positive staining of iNOS was seen in cytoplasm of smooth muscle cells and the activity of iNOS was elevated obviously (P<0. 01). (2) The intima hyperplasia was seen in splenic and gastric coronary vein, resulting in new intima and mimic atherosclerosis plaques, accompanied with hypertrophy of smooth muscle cells. The muscle fibers of veins were thickened obviously with an increase of extracellular matrix. There is a causal relationship between the portal hypertension and portal hypertensive vasculopathy.

关 键 词：血管病变 病理学 门脉高压症 

分 类 号：R657.34[医药卫生—外科学]