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目的 探讨川芎嗪对慢性低O2 高CO2 性肺动脉高压的预防作用及其作用机制。方法 将Sprague Dawley大鼠分为正常对照组 (A组 ) ,4wk低O2 高CO2 组 (B组 ) ,4wk低O2 高CO2 +川芎嗪组 (C组 ) ,采用透射电镜、图像分析、免疫组化、原位杂交等方法 ,研究川芎嗪对慢性低O2 高CO2 大鼠肺动脉平均压 (mPAP)、颈动脉平均压 (mCAP)、血清一氧化氮 (NO)、肺动脉显微和超微结构、肺动脉结构型一氧化氮合酶 (ceNOS)和诱导型一氧化氮合酶 (iNOS)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 (t=8 190 ,P <0 0 1) ,C组mPAP明显低于B组 (t=4 894,P <0 0 1) ,三组间mCAP差异无显著性 (P >0 0 5 ) ,血清NO浓度C组与B组相比明显增高 (t =2 196 ,P <0 0 5 ) ;②光镜下 ,肺细小动脉管壁面积 /管总面积比值(WA/TA)、肺细小动脉中膜平滑肌细胞核密度 (SMC)C组较B组明显降低 (t=4 815 ,P <0 0 1) ;电镜下 ,C组大鼠肺细小动脉中膜平滑肌细胞和胶原纤维增生较B组明显减轻 ;③免疫组化发现 ,C组肺细小动脉ceNOS的平均吸光度值较B组明显增高 (t =10 5 5 ,P <0 0 1) ;C组肺细小动脉iNOS的平均吸光度值与B组相比差异无显著性 (P >0 0 5 ) ;④原位杂交发现 ,C组肺细小动脉ceNOSmRNA平均吸光度值较B组明显?
Objective To explore the preventive effect of tetramethylpyrazine on chronic hypoxic hypercapnia with high CO2 and its mechanism of action. Methods Sprague Dawley rats were divided into normal control group (group A), 4wk low O2 high CO2 group (group B), 4wk low O2 high CO2 + ligustrazine group (group C), using transmission electron microscope, image analysis, and immunization group. By means of in situ hybridization and other methods to study the effects of tetramethylpyrazine on pulmonary artery mean pressure (mPAP), mean carotid artery pressure (mCAP), serum nitric oxide (NO), pulmonary artery microscopy, and ultrastructure in chronic hypoxic hypercapnia rats. Effects of cNOS, inducible nitric oxide synthase (iNOS) and its gene expression in pulmonary artery. Results The mean pulmonary arterial pressure (mPAP) in group 1B was significantly higher than that in group A (t=8 190, P<0.01). The mPAP in group C was significantly lower than that in group B (t=4 894, P < 0 01). There was no significant difference in mCAP between the two groups (P > 0.05). The serum NO concentration in group C was significantly higher than that in group B (t = 2 196, P < 0.05). 2 The area of pulmonary arterioles under light microscope The total area ratio (WA/TA) and the density of smooth muscle cells in the pulmonary arterioles (SMC) were significantly lower in group C than in group B (t = 4 815, P < 0 01); under electron microscope, the lungs in group C rats Fine arterial smooth muscle cells and collagen fibrosis were significantly less than those in group B.3 Immunohistochemistry showed that the average absorbance of ceNOS in group C was significantly higher than that in group B (t = 105, P <0 01). The average absorbance of iNOS in the pulmonary arterioles in group C was not significantly different from that in group B (P > 0.05). 4In situ hybridization revealed that the average absorbance of ceNOS mRNA in the small pulmonary arteries was significantly higher in group C than in group B.