摘要
目的:探讨低氧性肺动脉高压大鼠肺组织中尾加压素Ⅱ的合成、分泌及其在低氧性肺动脉高压病理生理过程中的作用。方法:实验选用雄性Wistar大鼠76只,随机分为正常对照组,低氧10,20,30d组,每组19只,在低氧10d和20d后各有1只死亡。间断常压低氧方法复制低氧性肺动脉高压大鼠模型,应用光镜、免疫组化、放射免疫分析等方法,测定低氧各组和对照组大鼠肺组织中尾加压素Ⅱ蛋白表达及血浆、支气管肺泡灌洗液尾加压素Ⅱ含量的动态变化。结果:各组大鼠支气管黏膜上皮细胞、肺血管内皮细胞及其平滑肌细胞、肺巨噬细胞、肺泡Ⅱ型上皮细胞和支气管软骨细胞中尾加压素Ⅱ均呈阳性表达,低氧后上述各种细胞中尾加压素Ⅱ表达明显增强。血浆和支气管肺泡灌洗液尾加压素Ⅱ浓度于低氧10d开始升高(4.26±1.61),(20.93±6.64)pmol/L,20d时两者均达高峰(9.03±1.80),(34.71±5.31)pmol/L明显高于对照组(3.74±1.08),(16.83±4.99)pmol/L(t=6.15,7.39,P<0.001),低氧30d出现下降趋势,但仍高于对照组(t=2.24,3.97,P<0.05)。结论:低氧可促进肺组织中尾加压素Ⅱ的合成和释放;在低氧性肺动脉高压病理生理过程中,尾加压素Ⅱ对调节肺循环和肺通气及肺血管改建等方面发挥重要作用。
AIM:To investigate the synthesis and secretion of urotensinⅡin the lung tissues of rats with hypoxic pulmonary hypertension(HPH), and to study mechanism and significance of urotensinⅡin the pathogenesis process of HPH. METHODS:Seventy-six male Wistar rats were randomly divided into normal control group and 10,20 and 30-day hypoxia groups,with 19 rats in each group,and there was 1 rat died 10 and 20 days after hypoxia respectively.The rat models of HPH were reproduced with normal barometric and discontinuous hypoxia.The expression of urotensinⅡprotein in lung tissues,dynamic changes of urotensinⅡcontent in plasma and bronchoalveolar lavage fluid were measured in the rats of the normal control group and hypoxia groups. RESULTS:Positive expressions of urotensinⅡwere observed in bronchial mucous membrane epithelial cells,pulmonary vascular endothelial cells and bronchial smooth muscular cells,pulmonary macrophages and type Ⅱalveolar epithelial cells and bronchial cartilage in all the groups.After hypoxia, the expression of urotensinⅡin the above cells were obviously increased.The urotensinⅡcontents in plasma and bronchia alveolar lavage fluid began to increase 10 days after hypoxia[(4.26±1.61),(20.93±6.64) pmol/L],and both reached the peak values 20 days after hypoxia[(9.03±1.80), (34.71±5.31) pmol/L],which were obviously higher than those in the control group[(3.74±1.08),(16.83±4.99) pmol/L] (t=6.15,7.39,P< 0.001),while they began to decrease 30 days after hypoxia, but still higher than those in the control group(t=2.24,3.97,P< 0.05). CONCLUSION:Hypoxia can promote synthesis and release of urotensinⅡin lung tissue, and urotensinⅡplays an important role in regulating pulmonary circulation and ventilation,and pulmonary vascular structural remodeling during the pathophysiological process of HPH.
出处
《中国临床康复》
CSCD
北大核心
2005年第15期99-101,共3页
Chinese Journal of Clinical Rehabilitation
