门静脉海绵样变大鼠门静脉氧化应激损伤的研究

The study on oxidative stress damage of portal vein involved in cavernous transformation of portal vein rats

目的:考察门静脉海绵样变性(CTPV,Cavernous transformation of portal vein)大鼠体内氧化应激的状态以及氧化应激对门静脉结构的影响。方法:采用门脉部分结扎法复制CTPV大鼠动物模型;通过测定门静脉内血浆超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活力来分析机体抗氧化能力,测定丙二醛(MDA)含量分析机体氧化能力;门静脉HE染色观察门静脉病理变化。结果:Sham组大鼠门静脉造影显示门静脉通畅,无曲张与扩张;门静脉病理学检查显示门静脉管腔无增大、内皮细胞光滑、中膜平滑肌层无增厚、外膜完整。CTPV组大鼠门静脉造影显示门静脉周围侧支循环形成,门静脉病理检查显示多个管腔大小不一、外形不规则血管腔,管腔之间为较狭窄的纤维性间隔,其内可见脂肪细胞、散在的淋巴细胞及肥大细胞等,门静脉管腔增大、血管内膜受损、内皮细胞脱落、中膜平滑肌增厚和血栓形成。与Sham组大鼠比较,CTPV组大鼠SOD、GSH-Px活性降低(93.79+8.87μU/L Vs103.05+8.07μU/L,P<0.05,157.44+26.46U/ml Vs709.09+83.21U/ml,P<0.05),而MDA含量增加(5.33+0.35μmol/L Vs3.59+0.44μmol/L,P<0.01)。结论:CTPV大鼠体内门静脉氧化应激状态增强;而增强的氧化应激可能与CTPV大鼠门静脉结构的损害有密切相关。

Objective： This study was designed to investigate oxidative stress status of cavernous transformation of portal vein （CTPV） and the influence of oxidative stress to structure of portal vein. Methods： The cavernous transformation of portal vein rat model was prepared by partial portal-vein ligation. Antioxidant capacities were evaluated by assaying activities of superoxide dismutase （SOD）, glutathione peroxidase（GSH-Px） in the portal vein blood. The content of malonaldehyde （MDA）,maker of lipid peroxidafion,was assayed as oxidative stress level in the portal vein blood. The portal veins were stained by hematoxylin-eosin staining to study their vascular pathological lesions. Results： Portography showed that the portal vein seemed smooth without variceal and dilatation in sham group. Pathological examination demonstrated that the portal vein walls were not enlarged, endothelial cells were smooth, the smooth muscle of middle membrane were not thickened and adventitia was intact. Portography showed that collateral circulation formed around portal vein in CTPV group, the vessel lumens with different size and irregular shapes were displayed by pathological examination. Within the narrow fibrous septum between there were the lumens the fat cells, scattered lymphocytes and mast cells, etc. The portal vein walls were enlarged notably, endothelial cells were damaged, the smooth muscle of middle membrane were thickened, thrombosis were formed. Total antioxidative capacity and activities of SOD and GSH-Px were remarkably decreased （93.79＋8.871a U/L Vs 103.05＋8.071.1 U/L, P 〈0. 05, 157.44＋26.46 U/ml Vs 709.09＋83.21 U/ml, P 〈0.05）,the content of MDA was increased in CTPV rats compared with sham rats （5.33＋0.35/a mol/L Vs 3.59＋0.44 p mol/L, P 〈0.01）. Conclusion： These findings suggest that the oxidative stress status of CTPV were enhanced and oxidative stress may contribute to portal vein structure damage in this rat model of CTPV.