首页> 外文期刊>International Journal of Clinical and Experimental Pathology >Contribution of calcium-activated chloride channel to elevated pulmonary artery pressure in pulmonary arterial hypertension induced by high pulmonary blood flow
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Contribution of calcium-activated chloride channel to elevated pulmonary artery pressure in pulmonary arterial hypertension induced by high pulmonary blood flow

机译:钙激活的氯离子通道对高肺血流量引起的肺动脉高压中肺动脉高压的贡献

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The correlation between calcium-activated chloride channel (CaCC) and pulmonary arterial hypertension (PAH) induced by high pulmonary blood flow remains uncertain. In this study, we investigated the possible role and effects of CaCC in this disease. Sixty rats were randomly assigned to normal, sham, and shunt groups. Rats in the shunt group underwent abdominal aorta and inferior vena cava shunt surgery. The pulmonary artery pressure was measured by catheterization. Pathological changes, right ventricle hypertrophy index (RVHI), arterial wall area/vessel area (W/V), and arterial wall thickness/vessel external diameter (T/D) were analyzed by optical microscopy. Electrophysiological characteristics of pulmonary arterial smooth muscle cells (PASMCs) were investigated using patch clamp technology. After 11 weeks of shunting, PAH and pulmonary vascular structural remodeling (PVSR) developed, accompanied by increased pulmonary pressure and pathological interstitial pulmonary changes. Compared with normal and sham groups, pulmonary artery pressure, RVHI, W/V, and T/D of the shunt group rats increased significantly. Electrophysiological results showed primary CaCC characteristics. Compared with normal and sham groups, membrane capacitance and current density of PASMCs in the shunt group increased significantly, which were subsequently attenuated following chloride channel blocker niflumic acid (NFA) treatment. To conclude, CaCC contributed to PAH induced by high pulmonary blood flow and may represent a potential target for treatment of PAH.
机译:由高肺血流量引起的钙激活氯离子通道(CaCC)与肺动脉高压(PAH)之间的相关性仍不确定。在这项研究中,我们调查了CaCC在这种疾病中的可能作用和影响。 60只大鼠随机分为正常,假和分流组。分流组的大鼠接受腹主动脉和下腔静脉分流手术。通过导管插入术测量肺动脉压力。通过光学显微镜分析病理变化,右心室肥大指数(RVHI),动脉壁面积/血管面积(W / V)和动脉壁厚度/血管外径(T / D)。使用膜片钳技术研究了肺动脉平滑肌细胞(PASMC)的电生理特性。分流11周后,出现PAH和肺血管结构重塑(PVSR),并伴有肺压升高和病理性肺间质改变。与正常和假手术组相比,分流组大鼠的肺动脉压,RVHI,W / V和T / D显着增加。电生理结果显示出主要的CaCC特性。与正常和假手术组相比,并联组中PASMC的膜电容和电流密度显着增加,随后在氯离子通道阻滞剂尼氟酸(NFA)处理后减弱。总之,CaCC有助于高肺血流量诱导的PAH,并且可能代表了治疗PAH的潜在目标。

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