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作 者:于忠和[1] 郝淑玲[1] 刘伯英[2] 尤兰华[1] 杜玉国[1]
机构地区:[1]北京军区总医院呼吸科,北京市100700 [2]中国人民解放军第251医院血液科
出 处:《中国全科医学》2008年第20期1847-1849,共3页Chinese General Practice
基 金:国家自然科学基金资助项目(30370632)
摘 要:目的揭示血管新型收缩肽——尾加压素Ⅱ(urotensinⅡ,UⅡ)在缺氧性肺动脉高压发生、发展中可能发挥的病理生理作用,探讨低氧对肺组织各种细胞成分UⅡ基因表达、合成和释放的影响。方法建立缺氧性肺动脉高压大鼠模型,采用免疫组织化学方法(IHC),观察UⅡ在不同低氧时间点大鼠肺组织各种细胞中的分布及变化。结果UⅡ在肺组织多种细胞中广泛分布。低氧后,UⅡ在肺组织各种细胞中表达增强。低氧10 d和20 d最明显。结论低氧可以促使肺组织中多种细胞合成、分泌UⅡ。低氧也促进肺组织UⅡ的释放。UⅡ参与缺氧性肺动脉高压的发生与发展。Objective To reveal the patho-physiological role of urotensin Ⅱ(UⅡ),a new vasoconstriction peptide,in the occurrence and development of hypoxic pulmonary hypertension(HPH),and to investigate the effects of hypoxia on UⅡ gene expression,synthesis and release in various cell components of pulmonary tissues.Methods HPH rat models were established using immunohistochemistry(IHC) to observe the distribution of UⅡ on various cell components of rat pulmonary tissues at different time points of hypoxia.Results UⅡ was widely distributed in a variety of pulmonary cells.Its expression was boosted in various cells of pulmonary tissues after appearance of hypoxia,especially in hypoxia 10 d and 20 d.Conclusion Hypoxia can promote many lung tissue cells to synthesize and excrete UⅡ,and lung tissue UⅡ to release,too.UⅡ participates in the occurrence and development of HPH.
分 类 号:R543[医药卫生—心血管疾病]
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