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目的研究川芎嗪对慢性低O2 和高CO2 致大鼠肺动脉高压及TXA2 和PGI2 的影响。方法30只SD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 ) ,观察川芎嗪对慢性低O2 高CO2 大鼠肺动脉平均压(mPAP)、颈动脉平均压(mCAP)、肺动脉显微和超微结构、血浆TXB2 及6_keto_PGF1α 浓度的影响。结果(1)B组mPAP明显高于A组(P<0.01) ,C组mPAP明显低于B组(P<0.01) ,三组间mCAP无明显差异(P>0.05) ;(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)B组较A组明显增高(P均<0.01) ,C组WA/TA、SMC较B组明显降低(P均<0.01) ,电镜下 ,B组肺细小动脉中膜平滑肌细胞增生 ,面积增大 ,染色质增多 ,外膜胶原纤维密集 ,C组大鼠肺细小动脉中膜平滑肌细胞和外膜胶原纤维增生较B组明显减轻 ;(3)B组TXB2 较A组明显增高(P<0.01) ,C组TXB2 较B组明显降低(P<0.01) ,6_keto_PGF1α 三组间无显著性差异(P>0.05) ,B组TXB2/6_keto_PGF1α 比值较A组明显增高(P<0.01) ,C组TXB2/6_keto_PGF1α 比值较B组明显降低(P<0.01)。结论川芎嗪抑制TXA2 合成可能为其抑制慢性低O2 和高CO2 性肺动脉高压及肺血管结构重建的作用机制之一
Objective To study the effects of tetramethylpyrazine on pulmonary hypertension and TXA2 and PGI2 in rats with chronic low-O2 and high-CO2. Methods Thirty male Sprague-Dawley rats were randomly divided into normal control group (group A), low wow O2 high CO2 group (group B), 4 wk low O2 high CO2+ tetramethylpyrazine group (group C), and tetramethylpyrazine was used to chronic low O2 high CO2. Mean pulmonary artery pressure (mPAP), mean carotid artery pressure (mCAP), pulmonary arterial microscopy and ultrastructure, plasma TXB2 and 6_keto_PGF1α concentrations. Results (1) The 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). There was no significant difference in mCAP between the three groups (P>0.05); (2) Light microscopy The ratio of pulmonary arterial wall area to total tube area (WA/TA), pulmonary arterioles smooth muscle cell nuclear density (SMC) in group B was significantly higher than that in group A (P<0.01), and group C WA/TA, SMC was significantly lower than that in group B (all P<0.01). Under electron microscope, the smooth muscle cells in the small arteries of the lungs in the group B proliferated, the area increased, the chromatin increased, and the outer membrane collagen fibers were dense. Smooth muscle cell and adventitia collagen fibrosis were significantly less than those in group B; (3) TXB2 in group B was significantly higher than that in group A (P<0.01). TXB2 in group C was significantly lower than that in group B (P<0.01). There was no difference between 6_keto_PGF1α groups. Significant difference (P>0.05), the ratio of TXB2/6_keto_PGF1α in group B was significantly higher than that in group A (P<0.01), and the ratio of TXB2/6_keto_PGF1α in group C was significantly lower than that in group B (P<0.01). Conclusion The inhibition of TXA2 synthesis by tetramethylpyrazine may be one of the mechanisms that inhibit the hypoxic and high CO2 pulmonary hypertension and pulmonary vascular structural reconstruction.