尾加压素Ⅱ在低氧性肺动脉高压中基因表达、合成、释放及意义的基础研究

The expression, synthesis and release of Urotensin Ⅱ in hypoxic pulmonary hypertension and its significance

目的探讨加压素Ⅱ（UⅡ）在低氧性肺动脉高压中基因表达合成释放的意义。方法本研究采用建立HPH大鼠模型，采用RIA观察不同低氧时间点大鼠血浆、支气管肺泡灌洗液（BALF）中UⅡ／、ADM含量的动态变化，从整体动物水平探讨低氧对UⅡ合成和释放的影响，以及UⅡ和ADM在HPH中的相互关系及意义；从而为揭示UⅡ在HPH中的病理生理作用提供实验依据。结果成功复制HPH动物模型；低氧促进肺组织UⅡ的表达、合成和释放；UⅡ参与HPH发病过程；在HPH发生发展过程中UⅡ和ADM之间存在正相关。结论两种血管活性肽具有相反的生理作用，推测二者之间的比例平衡对于调节肺循环和肺通气，稳定肺动脉压力具有非常重要的作用。

Objective To study the release of synthetic gene expression induced by vasopressin Ⅱ （ UⅡ ） in hypoxic pulmonary hypertension. Methods Rat model of HPH was establish. RIA was used to observe the different time points of hypoxia in plasma and the dynamic changes of U Ⅱ , ADM content in bronchoalveolar lavage fluid （BALF）. The impact of the release of U Ⅱ , as well as the relationship among U Ⅱ , ADM and HPH were explored to reveal the role of U Ⅱ in the pathophysiology of HPH. Results Rat HPH model was successfully established. Hypoxia promoted the expression, synthesis and release of U Ⅱ in lung tissue. U Ⅱ involved in the pathogenesis of HPH. HPH took place in the development of U Ⅱ and was positive correlated with ADM. Conclusion The two peptides have opposite physiological effects on blood vessel, which suggest that these two peptides play an important role in maintaining the balance between the pulmonary circulation and lung ventilation as well as the stability of pulmonary artery pressure.