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目的 :建立左向右分流所致肺动脉高压的大鼠模型 ,探讨高肺血流量对肺血流动力学及肺动脉平滑肌细胞增殖和凋亡的影响。方法 :采用腹主动脉 -下腔静脉分流术建立左向右分流的大鼠模型 ,观察术后 6周和 1 1周肺血流动力学 ,右心室肥厚和肺动脉舒张反应的改变。采用免疫组织化学和原位缺口末端标记方法对 1 1周组大鼠肺血管平滑肌细胞进行增殖和凋亡状态的研究。结果 :术后 6周与 1 1周大鼠肺动脉收缩压、肺动脉平均压、右心室 (RV)与左心室加室间隔 (LV +S)的比值较同龄对照组明显增加 ,而且 1 1周分流组肺动脉收缩压较 6周分流组进一步增高。在 1 1周分流组大鼠中 ,乙酰胆碱 (ACh)产生的肺动脉环舒张反应较对照组明显减弱 ,而硝普钠(SNP)产生的肺动脉环舒张百分比无明显变化。 1 1周分流组大鼠肺动脉平滑肌细胞增殖指数 (PI)、凋亡指数(AI)、PI/AI比值明显高于 1 1周对照组大鼠肺动脉平滑肌细胞。结论 :腹主动脉 -下腔静脉分流术可导致肺动脉高压形成。高肺血流量引起的内皮依赖性肺血管舒张功能失调对肺动脉高压的形成有重要的影响 ,肺动脉平滑肌细胞增殖的增加和凋亡的相对减少在肺动脉高压的发生中起重要作用。该模型简单、可靠、重复性好。
OBJECTIVE: To establish a rat model of pulmonary hypertension induced by left-to-right shunt and investigate the effects of high pulmonary blood flow on pulmonary hemodynamics and proliferation and apoptosis of pulmonary artery smooth muscle cells. Methods: The rat model of left-to-right shunt was established by abdominal aorta-inferior vena cava shunt. The changes of pulmonary hemodynamics, right ventricular hypertrophy and pulmonary vasodilation were observed at 6 and 11 weeks after operation. Immunohistochemistry and in situ nick end labeling were used to study the proliferation and apoptosis of pulmonary vascular smooth muscle cells in 11-week-old rats. Results: The pulmonary artery systolic pressure, mean pulmonary artery pressure, right ventricular (RV) and left ventricular septum (LV + S) ratio in 6 weeks and 11 weeks after operation were significantly higher than those in the same age control group, Pulmonary artery systolic blood pressure increased more than 6 weeks shunt group. In the shunt group at 11 weeks, the relaxation of pulmonary artery rings induced by acetylcholine (ACh) was significantly weaker than that of the control group, while the relaxation percentage of pulmonary artery rings produced by SNP did not change significantly. The proliferation index (PI), apoptotic index (AI) and PI / AI of pulmonary artery smooth muscle cells in 1-week shunt group were significantly higher than those in control group 1 week rat pulmonary artery smooth muscle cells. Conclusion: Abdominal aorta-inferior vena cava shunt can lead to the formation of pulmonary hypertension. Endothelium-dependent pulmonary vasodilation dysfunction caused by high pulmonary blood flow has an important effect on the formation of pulmonary hypertension. The increase of pulmonary artery smooth muscle cell proliferation and the relative reduction of apoptosis play an important role in the pathogenesis of pulmonary hypertension. The model is simple, reliable and reproducible.