摘要
目的:探讨内皮素-1(endothelin-1,ET-1)、一氧化氮(nitric oxide,NO)、降钙素基因相关肽(calcitonin gene-related peptide,CGRP)在大鼠肝肺综合征(hepatopulmonary syndrome,HPS)发病机制中的作用.方法:健康Wistar大鼠32只随机平均分为假手术组、CBDL术后3wk组、4wk组、5wk组.采用胆总管结扎(common bile duct ligation,CBDL)术制备大鼠HPS模型成功后,行肝功能及肝肺病理检查.放射免疫分析法检测大鼠血浆和肝组织、肺组织匀浆中ET-1和CGRP的水平,利用硝酸还原酶法检测大鼠血清和肝、肺组织匀浆中NO的水平.结果:在大鼠HPS形成过程中,肝细胞变性、坏死,大量纤维组织增生,形成假小叶.肺泡毛细血管增生、扩张,伴肺泡间隔增宽、容量减小.术后3-5wk,CBDL组大鼠血浆和肝、肺组织匀浆中ET-1、NO、CGRP水平显著升高,且与ALT水平呈正相关(血浆,ET-1:r=0.9889,P=0.0111;NO:r=0.9935,P=0.0065;CGRP:r=0.9714,P=0.0286;肝组织:r=0.9969,P=0.0035;r=0.9993,P=0.0070;r=0.9507,P=0.0493;肺组织:r=0.9939,P=0.0061;r=0.9991,P=0.0009;r=0.9557,P=0.0443).结论:在大鼠HPS形成过程中,血浆和肝、肺组织匀浆中ET-1,NO和CGRP水平持续升高,提示血管活性物质ET-1,NO和CGRP在其发病机制中可能起着一定作用.
AIM： To explore the roles of endothelin-1 （ET-1）, nitric oxide （NO） and calcitonin generelated peptide （CGRP） in the pathogenesis of hepatopulrnonary syndrome （lIPS） in rats.
METHODS： Thirty-two male Wistar rats were randomly and averagely divided into 4 groups： sham operation group, common bile duct ligation （CBDL） 3-wk group, CBDL 4-wk group and CBDL 5-wk group. HPS model was induced by CBDL. Liver function and pathological changes of liver and lung were observed. The concentrations of ET-1 and CGRP in plasma, liver and lung tissues were detected by radioimmunoas- say （RIA） and the NO content in serum, liver and lung tissues was measured with nitrate reductase method. RESULTS： During the pathogenesis of HPS, liver was damaged with inflammation and fibrous hyperplasia. Fibrosis caused the formation of false lobules. Lung structural alterations such as alveolar capillary dilation and angiogenesis, thickened alveolar septa and decreased alveolar capacity were observed. The levels of ET-1, NO and CGRP in plasma, liver and lung tissues were gradually increased from the 3^rd to 5^th wk after CBDL, which were positively correlated with alanine aminotransferase level （plasma, ET-1： r = 0.9889, P = 0.0111; NO： r = 0.9935, P = 0065; CGRP： r = 0.9714, P =, 0.0286; liver tissue： r = 0.9969, P = 0.0035; r = 0.9993, P = 0.0070; r = 0.9507, P = 0.0493; lung tissue： r = 0.9939, P = 0.0061; r = 0.9991, P = 0.0009; r = 0.9557, P = 0.0443）.
CONCLUSION： The levels of ET-1, NO and CGRP in plasma, liver and lung are increased markedly during the process of HPS formation, suggesting that vascular mediators such as ET-1, NO and CGRP may play important roles in the pathogenesis of HPS.
出处
《世界华人消化杂志》
CAS
北大核心
2008年第10期1053-1058,共6页
World Chinese Journal of Digestology
基金
黑龙江省教育厅科学技术研究资助项目
No.11511401
黑龙江省卫生厅资助项目
No.2005-360~~
关键词
肝肺综合征
内皮素-1
一氧化氮
降钙素
基因相关肽
放射免疫法
硝酸还原酶法
Hepatopulmonary syndrome
Endothe-lin-1
Nitric oxide
Calcitonin gene-related peptide
Radioimmunoassay
Nitrate reductase method
