【摘要】 目的:研究钙激活氯离子通道及其通道阻断剂尼氟灭酸(niflumic acid,NFA)i、ndaryloxyacetic acid(IAA-94)在苯福林(phenylephrine,PE)引起的肺动脉收缩中的作用。方法:常规离体血管灌流法检测肺动脉环张力;采用钙荧光探针(Fura-2/AM)负载急性酶分离法(胶原酶Ⅰ型和木瓜蛋白酶)获得的大鼠肺动脉平滑肌细胞(PASMCs),观察NFA和IAA-94对PE诱导的PASMCs胞浆游离钙离子浓度([Ca2+]i)的影响,用荧光分光光度计法检测[Ca2+]i。结果:钙激活氯离子通道阻断剂NFA和IAA-94可以舒张PE引起的肺动脉环收缩;NFA和IAA-94对KCl引起的血管收缩无影响;PE可以引起[Ca2+]i升高,NFA和IAA-94对PE诱导[Ca2+]i升高无影响。结论:钙激活氯离子通道在生理状态下与血管活性药(PE)引起的肺动脉张力变化有关,这为研究其在低氧肺血管收缩中的作用提供了新的线索。更多还原

【Abstract】 Aim: To investigate the role of calcium-activated chloride channels and the Cl-channel blockers niflumic acid（NFA） and indaryloxyacetic acid（IAA-94） in the regulation of vascular contraction induced by phenylephrine（PE）.Methods: The PE-induced contraction in rat pulmonary artery was observed by using routine blood vascular perfusion in vitro.The fluorescence Ca²⁺ indicator Fura-2/AM was used to observe intracellular free Ca²⁺ concentration([Ca²⁺]i) of rat pulmonary artery smooth muscle cells（PASMCs） which were obtained by the acute enzyme separation method（collagnase I plus papain） on NFA and IAA-94 effects on PE-induced contraction.Changes of [Ca²⁺]i in PASMCs were measured by spectrofluorometry.Results: The anion channel blockers NFA and IAA-94 produced inhibitory effects on PE-induced contractions in the pulmonary artery.NFA and IAA-94 negligibly affected the KCl-induced pulmonary artery contractions.PE could increase [Ca²⁺]i but NFA and IAA-94 negligibly affected it.Conclusion: Calcium-activated chloride channels contribute to the agonist-induced pulmonary artery contractions under physiological conditions,which may be a new clue to investigate the hypoxic pulmonary vasoconstriction.更多还原