论文部分内容阅读
目的 :探讨硫氮卓酮对慢性低O2 高CO2 大鼠肺动脉压力的影响及其作用机制。方法 :将Sprague -Dawley大鼠分为正常对照组 (A组 ) ,四周低O2 高CO2 组 (B组 ) ,四周低O2 高CO2 +硫氮卓酮组 (C组 ) ,采用透射电镜、图像分析、免疫组化、原位杂交等方法 ,研究硫氮卓酮对慢性低O2 高CO2 大鼠肺动脉平均压 (mPAP)、颈动脉平均压 (mCAP)及肺动脉显微和超微结构、肺动脉结构型一氧化氮合酶 (ceNOS)及其基因表达的影响。结果 :①B组肺动脉平均压 (mPAP)明显高于A组 (P <0 0 1) ,C组mPAP明显低于B组 (P <0 0 1) ,A组和B组mCAP无明显差异 (P >0 0 5 ) ,C组mCAP低于B组 (P <0 0 1) ;②光镜下 ,肺细小动脉管壁面积 /管总面积比值 (WA/TA)C组明显低于B组(P <0 0 1) ;电镜下 ,C组大鼠肺细小动脉内皮损伤、中膜平滑肌细胞和胶原纤维增生明显轻于B组 ;③免疫组化见C组肺细小动脉ceNOS的平均吸光度值明显高于B组 (P <0 0 1) ;原位杂交发现C组肺细小动脉ceNOSmRNA平均吸光度值明显高于B组 (P <0 0 1)。结论 :硫氮卓酮可抑制慢性低O2 高CO2 性肺动脉高压形成和肺血管结构重建 ,肺动脉ceNOS及其基因表达的增加为其重要作用机制 ,硫氮卓酮可能为治疗COPD、肺动脉高压伴高血压或室上性心律失常患者较为理想的药物。
Objective: To investigate the effect of diazepam on pulmonary arterial pressure in chronic hypoxic hypercapnic rats and its mechanism. Methods: Sprague-Dawley rats were divided into normal control group (group A), low O2 high CO2 group (group B), low oxygen high CO2 + diazoxide group (group C) (MPAP), mean arterial pressure (mCAP), pulmonary arterial microstructure and ultrastructure, pulmonary artery structure Type nitric oxide synthase (ceNOS) and its gene expression. Results: (1) The mean pulmonary arterial pressure (mPAP) in group B was significantly higher than that in group A (P <0.01); the mPAP in group C was significantly lower than that in group B (P <0.01) (P <0.01). (2) Under light microscopy, the ratio of wall area / total tumor area (WA / TA) of pulmonary arterioles in group C was significantly lower than that in group B P <0.01). Under the electron microscope, the endothelial cell injury of pulmonary arterioles, proliferation of mesangial smooth muscle cells and collagen fibers in group C were significantly lower than those in group B. ③ The average absorbance of ceNOS in group C was significantly higher than that in group B (P <0.01). In situ hybridization showed that the average absorbance of ceNOS mRNA in group C was significantly higher than that in group B (P <0.01). Conclusion: Azithromycin can inhibit the formation of chronic hypoxic hypercapnic pulmonary hypertension and pulmonary vascular remodeling. The increase of ceNOS and its gene expression in pulmonary arteries may play an important role in the treatment of COPD and pulmonary hypertension. Blood pressure or supraventricular arrhythmias are the ideal drug.