【摘要】 目的研究钙激活氯离子(ClCa)通道阻滞剂尼氟灭酸(NFA)对急性低氧人肺动脉收缩的影响。方法在常氧(37℃、5%CO2、21%O2、74%N2)和急性低氧(37℃、5%CO2、2%O2、93%N2)条件下,采用荧光分光光度计法、离体血管灌流法,观察ClCa阻滞剂NFA和indaryloxyacetic acid(IAA-94)对急性低氧人肺动脉平滑肌细胞质内游离钙离子浓度([Ca2+]i)及肺动脉张力的影响。结果①急性低氧引起[Ca2+]i升高,由常氧时的(103.26±4.72)nmol.L-1升高至(253.89±9.82)nmol.L-1(P<0.01);加入NFA、IAA-94使[Ca2+]i明显下降,最低至(107.18±14.99)nmol.L-1(P<0.01);②急性低氧引起肺动脉环收缩,由常氧时的(4.54±0.52)g.g-1至最大收缩张力(49.51±1.30)g.g-1(P<0.01);加入NFA和IAA-94后,它们均能抑制由低氧引起的血管收缩,使收缩张力最低降至(4.50±0.40)g.g-1(P<0.01)。结论 NFA能有效抑制急性低氧引起的肺动脉收缩,这一效果可能是通过抑制ClCa通道活性来实现的。更多还原

【Abstract】 Aim To investigate the effects of nifiumic acid(NFA),an inhibitor of calcium-activated chloride(ClCa)channels,on pulmonary vasoconstriction of human in acute hypoxic conditions.Methods Acute hypoxia-induced contraction was observed in human pulmonary artery by using routine blood vascular perfusion in vitro;the fluorescence Ca2+ indicator Fura-2/AM was used to observe intracellular free Ca2+ concentration(i) in human pulmonary artery smooth muscle cells(PASMCs)through putting into ClCa channel blockers NFA and indaryloxyacetic acid(IAA-94)in normal(37℃,5% CO2,21% O2,74% N2)and acute hypoxic(37℃,5% CO2,2% O2,93% N2)conditions.Results ① In acute hypoxic condition,i was increased:in normoxic condition,i was(103.26±4.72)nmol·L-1,and in hypoxic condition,i was(253.89±9.82)nmol·L-1(P<0.01);The NFA and IAA-94 decreasedi from(253.89±9.82)nmol·L-1 to(107.18±14.99)nmol·L-1(P<0.01).② Acute hypoxia evoked pulmonary artery contractions from(4.54±0.52)g·g-1 to(49.51±1.30)g·g-1(P<0.01);The NFA and IAA-94 inhibited hypoxia-evoked contractions in the pulmonary artery from(49.51±1.30)g·g-1 to(4.50±0.40)g·g-1(P<0.01).Conclusions NFA can inhibit the contraction of human pulmonary artery in acute hypoxic condition,which may result from the inhibition of activity ClCa channels.更多还原