| 氯离子通道阻滞剂通过抑制MAPK通路减轻低氧高二氧化碳性肺血管收缩 |
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| 引用本文： | 黄林静,王淑君,何金波,马迎春,应磊,陈锡文,王万铁.氯离子通道阻滞剂通过抑制MAPK通路减轻低氧高二氧化碳性肺血管收缩[J].温州医学院学报,2014(1):15-19. |
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| 作者姓名： | 黄林静 王淑君 何金波 马迎春 应磊 陈锡文 王万铁 |
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| 作者单位： | [1]温州医科大学病理生理学教研室,浙江温州325035 [2]赤峰上京内分泌专科医院,内蒙古赤峰024000 [3]温州医科大学实验动物中心,浙江温州325035 |
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| 基金项目： | 浙江省自然科学基金资助项目（Y2080760）;浙江省中医药重点学科建设计划项目（2012-XK-A28）. |
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| 摘 要： | 目的：探究氯离子通道阻滞剂尼氟灭酸对低氧高二氧化碳性肺血管收缩（HHPV）的影响及与MAPK信号通路的关系。方法：采用大鼠HHPV模型，将所有二级肺动脉环随机分为：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）、尼氟灭酸＋SB203580组（NFA＋SB组）、尼氟灭酸＋U0126组（NFA＋U组），按照低氧高二氧化碳反应性测定的方法测定各组肺动脉环的张力变化。结果：NFA＋SB组、NFA＋U组二级肺动脉环的收缩峰值较HD组均明显下降（P〈0．05和尸〈0．01），但I期快速收缩和I期快速舒张均无明显差异（均P〉0．05）；NFA＋SB组的收缩峰值较NFA组明显下降（P〈0．05），但NFA＋U组的收缩峰值较NFA组无明显变化（P〉0．05）。结论：氯离子通道阻滞剂可通过抑制MAPK信号通路，减轻二级肺动脉环Ⅱ期持续性收缩，并逆转为舒张状态，从而发挥拮抗HHPV的作用。
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| 关 键 词： | MAPK通路 低氧高二氧化碳 肺血管收缩 氟离子通道 大鼠 |
The blocker of chloride channels attenuated hypoxic hypercapnia pulmonary vasoconstriction through inhibiting MAPK signal pathway in rats |
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| HUANG Linjing,WANG Shujun,HE Jinbo,MA Yingchun YING Lei,CHEN Xiwen,WANG Wantie.The blocker of chloride channels attenuated hypoxic hypercapnia pulmonary vasoconstriction through inhibiting MAPK signal pathway in rats[J].Journal of Wenzhou Medical College,2014(1):15-19. |
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| Authors: | HUANG Linjing WANG Shujun HE Jinbo MA Yingchun YING Lei CHEN Xiwen WANG Wantie |
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| Institution: | 1.Department of Pathophysiology, Wenzhou Medical University, Wenzhou,325035; 2. Chifeng Shangjing Incretion Specialist Hospital, Chifeng, 024000; 3. The Animal Center of Wenzhou Medical University, Wenzhou, 325035) |
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| Abstract: | Objective： To investigate the effect of chloride channels and MAPK signal pathway in thepathological process of hypoxia hypercapnia-induced pulmonary vasooonstriction in rats. Methods： The model of hypoxia hypercapnia-induced pulmonary vasoconstriction rats was used, and the second branch pulmonary artery rings were randomly divided into： control group （N group）, hypoxia hypercapnia group （H group）, DMSO incubation group （HD group）, niflumic acid incubation group （NFA group）, niflumic acid＋SB203580 incubation group（NFA＋SB group）, niflumic acid＋U0126 incubation group （NFA＋U group）, the values of rings＇ tension change were recorded via the method of hypoxia hypercapnia conditions reactivity. Results： The second pulmonary artery rings incubated by NFA＋SB and NFA＋U group who＇s phase 1I persis- tent vasoconstrictive peak were significantly attenuated and then turn to vasodilatation compared with the HD group （P〈0.05 and P〈0.01） but the Phase I acute vasoconstriction and the Phase I vasodilation had no changes compared with HD （P〉0.05）; The second pulmonary arte（y rings incubated by NFA＋SB group who＇s vasocon- strictive peak was significantly attenuated compared with the NFA group （P〈0.05）, but the NFA＋U group didn＇t change （P〉0.05）. Conclusion： Chloride channel blocker can inhibit MAPK signaling pathway, reduces the second branch pulmonary artery rings＇ phase H sustained contraction, and reversed diastolic state, so as to play the role of HHPV antagonists. |
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| Keywords: | MAPK signal pathway hypoxia hypercapnia pulmonary vasoconstriction chloride channel rats |
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