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目的 研究在不同程度的充血性心力衰竭时肺脏水通道蛋白 1和 5 (AQP1、AQP5 )和上皮性钠通道(ENaC)表达的情况。方法 将SD大鼠通过腹主动脉 下腔静脉穿刺造瘘和冠脉结扎的方法建成不同的心衰模型。用Doppler超声心动图的方法比较其心功能的各项参数 ,用肺湿 /干质量比和肺脏组织学检查了解各组大鼠肺水肿的情况 ,并以RT PCR的方法检测肺脏AQP1、AQP5和ENaCα亚基的基因表达。结果 穿刺造瘘大鼠心功能损害较轻 ,而冠脉结扎大鼠心功能严重失代偿。各组大鼠肺湿 /干重比无显著性差异 ,但肺脏组织学检查显示冠脉结扎大鼠存在轻度的肺水肿。分子生物学检测发现冠脉结扎大鼠肺脏AQP1和αENCmRNA表达上调 (AQP1:1.4 88vs 0 .775 ,P <0 .0 0 1;αENaC :0 .5 2 4vs 0 .30 6 ,P <0 .0 5 ) ,而AQP5mRNA表达在各组大鼠之间未见显著性差异。结论 在严重的充血性心力衰竭大鼠肺脏存在着AQP1和ENaC基因表达的上调 ,其中AQP1表达增加可能参与了心源性的肺脏液体转运障碍
Objective To investigate the expression of aquaporin 1 and 5 (AQP1, AQP5) and epithelial sodium channel (ENaC) in patients with congestive heart failure. Methods Different models of heart failure were established in SD rats by puncturing the inferior vena cava of the abdominal aorta and ligating the coronary artery. Doppler echocardiography was used to compare the parameters of cardiac function, lung wet / dry mass ratio and lung histology were used to understand the pulmonary edema in rats. RT-PCR was used to detect the expression of AQP1, AQP5 and ENaC alpha subunit gene expression. Results The puncture-induced fistula was less damaged in cardiac function, but the cardiac function in rats with coronary artery ligation was severely decompensated. There was no significant difference in the lung wet / dry weight ratio of rats in each group, but the lung histological examination showed mild pulmonary edema in rats with coronary artery ligation. The results of molecular biology showed that the expressions of AQP1 and αENCmRNA in the lungs of rats with coronary artery ligation were up-regulated (AQP1: 1.488vs0.7775, P <0.01; αENaC: 0.244vs0.360, P < 5), while AQP5 mRNA expression was not significantly different between the groups of rats. Conclusions There is an up-regulation of AQP1 and ENaC gene expression in the lungs of rats with severe congestive heart failure. The increased expression of AQP1 may be involved in cardiogenic pulmonary fluid transport disorder