大鼠布-加综合征模型经尾静脉注入重组血管内皮生长因子促血管再生的研究  

Vascular regeneration by injection of recombinant vascular endothelial growth factor into vaginal muscular brachial plexus syndrome model via tail vein in rats

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作  者:张开明[1] 朱荣涛[1] 黄帅[1] 王维杰[1] 秦文杰[1] 孙玉岭[1] 

机构地区:[1]郑州大学第一附属医院肝胆胰外科,450052

出  处:《中华实验外科杂志》2017年第7期1129-1132,共4页Chinese Journal of Experimental Surgery

基  金:郑州市科技局科技人才队伍建设-科技领军人才项目(131PLJRC658)

摘  要:目的探讨血管内皮生长因子(VEGF)对布-加综合征(B-CS)大鼠的作用及其机制。方法采用雄性SD大鼠,手术缩窄肝上段下腔静脉的30%,4周后建成B-CS大鼠模型。实验分为假手术组(A组,n=15)、B-CS+VEGF组(B组,n=12)和B-CS+生理盐水组(C组,n=12)。B组持续尾静脉注射VEGF 6 μg/(kg·d),A、C两组注射等量生理盐水4周。于术后8周测定门静脉压力,苏木素-伊红(HE)染色观察肝组织病理学变化,免疫组织化学染色定量肝内外血管密度。结果大鼠B-CS成模率约60%,B-CS大鼠均出现肝后下腔静脉及主肝静脉梗阻,肝、脾淤血肿大,肠系膜淤血水肿,腹壁静脉和门静脉扩张,门静脉压力升高[A组:(10.00±0.38) mmHg(1 mmHg=0.133 kPa);B组:(15.50±0.59) mmHg;C组:(17.25±0.48) mmHg]。对比生理盐水组(2.80±0.38),VEGF组(8.20±0.53)增加B-CS大鼠肝内及食管胃底周围侧枝血管新生(P=0.000),明显降低B-CS门静脉压力,减少腹水(P=0.016),减轻肝细胞气球样变性(P=0.007)和肝脾淤血(P=0.028)。结论VEGF可通过促进肝内外侧枝血管新生,改善B-CS大鼠门静脉高压症。Objective To explore the effect of vascular endothelial growth factor (VEGF) on portal pressure in rats with Budd-Chiari syndrome (B-CS).Methods Male Sprague-Dawley (S-D) rats were used to make 30% narrow of the inferior vena cava by surgery. The experiments were divided into B-CS + VEGF group (group B, n=12), B-CS + normal saline group (group C, n=12) and sham operation group (group A, n=15). The animals in group B received continuous intravenous injection of VEGF (6 μg/kg body weight every day), and those in group A and C were given the same amount of normal saline for 4 weeks. The portal vein pressure was measured at 8th week postoperatively. Pathological changes of the liver were observed by HE staining. Intrahepatic vascular density was quantified by immunohistochemical staining.Results The rate of B-CS formation in rats was about 60%. B-CS rats showed obstruction of inferior vena cava and main hepatic vein, the swelling of the liver and spleen, the congestion of the mesentery, the enlargement of the abdominal vein and portal vein, and significantly elevated portal vein pressure [group A: (10.00±0.38) mmHg(1 mmHg=0.133 kPa); group B: (15.50±0.59) mmHg; group C: (17.25±0.48) mmHg, P=0.016], reduced the balloon degeneration of liver cell (P=0.007). As compared with the saline group (2.80±0.38), the collateral vessel angiogenesis was significantly increased in the liver and esophagus and gastric fundus (8.20±0.53, P=0.000). Portal vein pressure reduced, and ascites decreased, the balloon degeneration of liver cells, and liver and spleen congestion (P=0.028) alleviated in the VEGF group.Conclusion VEGF can improve the portal hypertension in B-CS rats by promoting angiogenesis in the medial and lateral branches of the liver.

关 键 词:布-加综合征 门静脉高压症 血管内皮生长因子 

分 类 号:R-332[医药卫生] R575

 

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