Conclusion Nitric oxide inhibited PDGF expression by pulmonary arteries of rats with hypoxic pulmonary vascular remodeling.
结论一氧化氮对缺氧性肺血管结构重建大鼠肺动脉中PDGF表达有抑制作用。
Conclusion Carbon monoxide inhibited TGF expression by pulmonary arteries of rats with hypoxic pulmonary vascular remodeling.
结论一氧化碳对缺氧性肺血管结构重建大鼠肺动脉中TGF表达有抑制作用。
Conclusions: the CTGF may play an important role in the pathogenesis process of hypoxic pulmonary vascular remodeling and pulmonary hypertension.
结论低氧所致CTGF的合成增多在低氧性肺血管重建和肺动脉高压的发病过程中起一定的作用。
Objective to investigate the impact of transforming growth factor (TGF) in the mechanisms by which carbon monoxide (CO) regulates hypoxic pulmonary vascular remodeling.
目的探讨一氧化碳对缺氧性肺血管结构重建大鼠肺动脉中转移生长因子(TGF)表达的影响。
The basic pathological alteration of pulmonary hypertension involves three dependent elements:pulmonary vasoconstriction, pulmonary vascular remodeling and pulmonary microvascular thrombogenesis.
前言：肺动脉高压的基本病理改变有三个方面：肺血管收缩、肺血管重构和肺小血管内微血栓形成。
Microstructure and ultrastructure of pulmonary arteries changed obviously in hypoxic rats with the development of hypoxic pulmonary vascular structural remodeling.
低氧组大鼠肺血管显微及超微结构发生明显改变，有肺血管结构重构形成。
Pulmonary vascular smooth muscle cell is an important executor of vasoconstriction and a key contributor of pulmonary vascular structure remodeling.
肺血管平滑肌细胞是肺血管收缩反应的主要执行者，也是肺血管结构重建的重要参与者。
Results: Pulmonary vascular structural remodeling developed after 2 week hypoxia.
结果：低氧2周后出现大鼠肺血管结构重建。
CONCLUSION: Feixin mixture reverses partially the remodeling of pulmonary vascular structure and reduces effectively pulmonary hypertension.
结论：肺心合剂能部分逆转肺血管结构重建，有效降低肺动脉高压。
Objective To establish a rat model of pulmonary hypertension induced by left-to-right shunt and explore the influence of high pulmonary blood flow on pulmonary vascular collagen remodeling.
目的建立左向右分流所致肺动脉高压大鼠模型，了解高肺血流量对肺血管胶原代谢的影响。
To investigate the role of vascular endothelial growth factor (VEGF) in remodeling of pulmonary arteries in rat with CB and emphysema during normoxic period.
研究血管内皮生长因子(VEGF)在慢支与肺气肿肺动脉重构中的作用。
Conclusion: the endoplasmic reticulum stress-induced apoptosis may be one of the mechanism of hypoxic pulmonary hypertension and pulmonary vascular wall remodeling.
结论：内质网应激介导的凋亡与大鼠慢性低氧性肺动脉高压、肺血管改建的病理过程有关。
Conclusion: the endoplasmic reticulum stress-induced apoptosis may be one of the mechanism of hypoxic pulmonary hypertension and pulmonary vascular wall remodeling.
结论：内质网应激介导的凋亡与大鼠慢性低氧性肺动脉高压、肺血管改建的病理过程有关。
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