钙敏感受体在高肺血流性肺动脉高压线粒体损伤中的作用  

The impact of Calcium-sensing receptor on the mitochondrial damage in high pulmonary blood flow in rats with pulmonary hypertension

作　　者：赵文[1] 郑宝石[1] 黄国雄[1] 宋绍辉[1] 覃家锦[1] 

机构地区：[1]广西医科大学第一附属医院胸心外科,南宁530021

出　　处：《中华实验外科杂志》2013年第4期746-748,共3页Chinese Journal of Experimental Surgery

基　　金：广西科学技术厅科技攻关与新产品试制项目资助课题（0816004-3）

摘　　要：目的观察钙敏感受体（CaSR）对高肺血流性肺动脉高压大鼠肺动脉线粒体功能的影响，并探讨其在高肺血流性肺动脉高压形成的作用机制。方法行左肺切除手术建立大鼠肺动脉高压模型。将27只大鼠随机分为3组（n=9），对照组、手术组、手术＋钙敏感受体阻滞剂Calhex231组。饲养35d后，检测各组大鼠肺动脉CaSRmRNA的表达；透视电镜观察肺动脉线粒体超微结构；原位末端转移酶标记（TUNEL）法统计各组大鼠内皮细胞凋亡率。结果大鼠肺动脉内皮细胞CaSRmRNA的相对表达量以2-△△Ct表示，对照组为0．0003±0．0001，手术组为0．0071-4-0．0041，手术＋Calhex231组为0．0011±0．0003，差异有统计学意义（P〈0．05）。与对照组比较，手术组肺动脉线粒体膜肿胀，线粒体活力下降，肺动脉内皮细胞凋亡率均明显升高（P〈0．05）；与手术组比较，手术＋Calhex231组线粒体膜肿胀度减轻，活力有所恢复，肺动脉内皮细胞凋亡率明显降低（P〈0．05）。结论高肺血流量可引起大鼠肺动脉内皮细胞CaSR的活化，进而调控线粒体途径，诱发肺动脉内皮细胞凋亡，引起肺动脉高压。Objective To observe the calcium-sensing receptor （CaSR） high pulmonary blood flow in rats with pulmonary hypertension pulmonary mitochondrial function, and to explore the mechanism of the formation Of its high pulmonary blood flow in pulmonary hypertension. Methods Row left lung re- section establish a rat model of pulmonary hypertension. 27 rats were randomly divided into 3 groups （n = 9）, the control group, the surgery group, surgery calcium-sensing receptor blockers Calhex231 group. Rats mean pulmonary artery pressure were measured after feeding 35d detect right ventricular/body weight （ right ventricle/body weight, RV/BW） and right ventricular/left ventricular interventricular septum （ right ventri- cle/left and lodging to plus septum, RV/LV S） ratio. The test groups the rat pulmonary CaSR mRNA ex- pression; mitochondrial uhrastructure; perspective electron-microscope pulmonary the TdT-mediated dUTP nick end labeling （TUNEL） method statistics rats in each group rate of endothelial cell apoptosis. Results Rat pulmonary artery endothelial cells CaSR mRNA relative expression levels of 2-△△Ct the control group compared with the control group 0. 0003 ＋ 0. 0001,0. 0071 ＋ 0. 0041, the surgery group difference was sta- tistically significant （ P 〈 0. 05 ） ; surgery group pulmonary mitochondrial membrane swelling, mitochondrial activity decreased pulmonary endothelial cell apoptosis was significantly increased （P 〈 0. 05 ）. The surgery Calhex231 rats pulmonary CaSRmRNA relative expression level of 0. 0011 ＋ 0. 0003, compared with the surgery group decreased significantly （P 〈 0. 05 ）, and reduce the swelling of the mitochondrial membrane, vitality has been restored, the pulmonary endothelial cell apoptosis rate was significantly lower （P 〈 0. 05 ）. Conclusion The high pulmonary blood flow can cause the activation of rat pulmonary artery endo- thelial cells CaSR regulating mitochondrial pathway to induce apoptosis of pulmonary artery endothelial cells, causing pulm

关 键 词：钙敏感受体 高肺血流 肺动脉高压 平滑肌 

分 类 号：R544.16[医药卫生—心血管疾病]