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作 者:薛必成[1] 陈少贤[1] 龚永生[2] 徐正祄[3] 王良兴[1] 范小芳[2] 胡良刚[3]
机构地区:[1]温州医学院第一附属医院呼吸内科,浙江温州325000 [2]温州医学院肺心病研究室,浙江温州325000 [3]温州医学院病理生理学教研室,浙江温州325000
出 处:《温州医学院学报》2005年第6期446-448,共3页Journal of Wenzhou Medical College
基 金:浙江省教育厅科研基金(20020468)
摘 要:目的:研究大鼠尾加压素Ⅱ(U-Ⅱ)收缩大鼠离体肺主动脉环与钙离子通道的关系。方法:从雄性Sprague-Dauley大鼠中分离出肺主动脉,切成3~4mm的血管环。用大鼠U-Ⅱ(30 nmol/L)预收缩血管达平台期后,加入钙离子通道阻断剂尼群地平,制备尼群地平(0.1~30μmol/L)浓度-效应舒张曲线,分别计算EC_(50)和Emax。结果:尼群地平可浓度依赖性舒张大鼠U-Ⅱ预收缩的肺主动脉环[-log(EC_(50))=5.86±0.30,Emax=(73.73±15.40)%,以30 nmol/L U-Ⅱ的收缩幅度为100%]。结论:钙离子通道的激活参与大鼠U-Ⅱ收缩大鼠肺主动脉效应。Objective: To investigate the relationship between rat urotensin- Ⅱ-induced contraction in rat main trunk of the pulmonary arteries and the activation of Ca^2+ channel. Methods: The main trunk of the pulmonary artery was dissected in the male Sprague-Dawley rat and cut into arterial ring in 3~4 mm width. Inhibitor of Ca^2+, nitrendipine (0.1 ~ 30 μmol/L) was added into the incubation medium after rat U- Ⅱ (30 nmol/L) induced contraction reached plateau to prepare the relaxant concentration-response curves. Their EC50 and Emax were calculated, respectively. Results: Nitrendipine could relax concentration-dependently the arterial rings of the rat U- Ⅱ precontracted arteries [-log[EC50]=5.86± 0.30, Emax=(73.73±15.40%) of the response to 30 nmol/ L rat U-Ⅱ ]. Conclusion: The activation of Ca^2+ participates in the response of rat U-Ⅱ-induced contraction of the main trunk of the pulmonary artery.
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