钙敏感受体与内源性一氧化氮在致大鼠高肺血流性肺动脉高压形成中的意义  

Significance of the calcium-sensing receptor and NO in the formation of high pulmonary blood flow derived pulmonary arterial hypertension in rat

作　　者：宋绍辉[1] 黄国雄[1] 赵文[1] 郑晓宇[2] 覃家锦[1] 

机构地区：[1]广西医科大学第一附属医院心胸外科,南宁530021 [2]广西南宁市第一人民医院心胸外科,南宁530021

出　　处：《微创医学》2013年第3期256-258,共3页Journal of Minimally Invasive Medicine

基　　金：广西科技攻关与新产品试制项目(合同号:0816004-3)

摘　　要：目的探讨钙敏感受体(CaSR)与内源性一氧化氮在致大鼠高肺血流性肺动脉高压形成中的机制。方法将24只SD大鼠随机分为实验组即肺动脉高压组(PAH组)和对照组,实验组行左肺切除手术。饲养30 d后,用右心导管法分别测定两组大鼠肺动脉平均压;检测右心室/体重(right ventricle/body weight,RV/BW)和右心室/左心室+室间隔(right ventricle/left ventricle plusseptum,RV/LV+S)比值,并以光学显微镜观测肺血管结构的变化,同时检测血浆一氧化氮(nitricoxide,NO)含量。应用RT PCR方法检测两组大鼠肺动脉内皮细胞CaSR mRNA的表达。结果 PAH大鼠肺动脉平均压(PAMP)、RV/BW及RV/(LV+S)比值均明显高于对照组(P<0.05),光镜下肺小动脉内皮细胞明显增生,中膜厚度明显增加(P<0.05),同时检测出PAH肺动脉内皮细胞的表达,亦比对照组明显增高(P<0.05);PAH组大鼠血浆中NO含量比对照组明显升高(P<0.05)。结论高肺血流时肺动脉内皮细胞CaSR mRNA表达的改变可能通过改变NO的产生和损伤线粒体等途径参与肺动脉高压的形成。] Objective To investigate the calcium-sensing receptor （CaSR） and endogenous NO in the mechanism of the formation of high pulmonary blood flow derived pulmonary hypertension in rat. Method 24 SD rats were randomly divided into pulmonary arterial hypertension group （ PAH group） or the con- trol group, with the PAH group were carried out with left lung resection surgery. After 30 day feeding, pulmonary artery mean pressure （PAMP） were measured by right heart catheterization, right ventricular weight / body weight （right ventricle / body weight, RV / BW） and right ventricle / left ventricle ＋ interventricular septum （right ventricle / left ventricle plus septum, RV / LV ＋ S） ratio were calculated, pulmonary vascular structural changes were observed with optical micro- scope, plasma NO were detected, and the expression of CaSR mRNA in pulmonary artery endotheli- al cell were detected by real-time quantitative PCR in both groups. Results PAMP, the RV / BW and RV / （ LV ＋ S to） the ratio in PAH group were significantly higher （P 〈 0.05） than those in the control group. Under light microscope, endothelial cell in pulmonary small artery proliferated obviously and the medium membrane thickness increased significantly in PAH group compared to those in the control group. Both the expression of CaSR mRNA in pulmonary artery endothelial celland plasma NO were apparently higher in PAH group than those in the control group. （all P 〈 0.05 ）. Conclusion The change in the expression of CaSR mRNA in pulmonary artery endothelial cell with high pulmonary blood flow might involve in the formation by changing the generation of NO and damaging mitochond6um. of pulmonary artery hypertension

关 键 词：钙敏感受体 高肺血流 肺动脉高压 一氧化氮 线粒体NO合酶 

分 类 号：R363[医药卫生—病理学]