尼氟灭酸在大鼠低氧高二氧化碳性肺血管收缩中的作用

目的：探讨氯离子通道阻断剂一尼氟灭酸（NFA）在大鼠低氧高二氧化碳性肺血管收缩（HHPV）中的作用。方法：采用大鼠HHPV模型，二、三级动脉环分别随机分4组（n=8）：常氧组（N组）、低氧高二氧化碳组（H组）、DMSO组（HD组）、尼氟灭酸组（NFA组）。在急性低氧高二氧化碳介质中，采用NFA分别孵育肺二、三级肺动脉环，按照低氧高二氧化碳反应性测定的方法测定其二、三级肺动脉血管环张力的变化，并观察NFA对HHPV的影响。结果：①H组二、三级肺动脉均呈现双向性收缩变化（I期快速收缩、快速舒张；II期持续性收缩）与N组相比有显著性差异（P〈0．05，P〈0．01）；②NFA组二、三级肺动脉环的低氧高二氧化碳性血管收缩作用明显减弱，尤其是Ⅱ期的持续收缩，与HD组相比有显著性差异（P〈0．05，P〈0．01）。结论：氯离子通道阻断剂一尼氟灭酸可减轻大鼠二、三级肺动脉环的张力变化率（尤其是Ⅱ期的持续性收缩），从而发挥拮抗HHPV的作用。

The effect of niflumic acid in hypoxic hypercapnia pulmonary vasoconstriction

Objective： To investigate the effect of chloride channel blocker--nitlumic acid（NFA）on the pathological process of hypoxia hypercapnia-induced pulmonary vasoconstriction in rats. Methods： We used the model of hypo~da hypercapnia-induced pulmonary vasoconstric- tion rats, and divided the second, third branch pulmonary artery rings randomly into four groups（ n = 8） ：control group（N group）, hypoxia hy- percapnia group（H group）, DMSO incubation group（I-ID group）, niflumic acid group（NFA group）. Under acute hypoxia hypercapnia condi- tions, we observed the effects of the three stages of hypoxia hypercapnia-induced pulmonary vasoconstriction（HHPV） incubated by NFA in the second,third brach pulmonary artery rings. At the same time , the values of rings＇ tension changings were recorded via the method of hypoxia hypercapnia conditions reactivity. And investigated the effect of NFA to HHPV. Results： （i） Under the hypoxia hypercapnia condition , we ob- served a biphasic pulmonary artery contractile（the phase I rapid contraction and vasodilation; the phase II sustained contraction） response in both the second and the third branch pulmonary artery rings compared with the control group （ P 〈 0.05 , P 〈 0.01） ; QThe second and third pulmonary artery rings incubated by NFA which phase II persistent vasoconstriction were significantly attenuated compared with the H group （P 〈 0.05 , P 〈 0.01）. Conclusion： The blocker of the chloride channels attenuates the second and third branch pulmonary artery rings constriction in rat, especially the phase II persistent vasoconstriction, so then have an antagonistic effect on HHPV.