The blocker of chloride channels attenuated hypoxic hypercapnia pulmonary vasoconstriction through inhibiting MAPK signal pathway in rats

Objective: To investigate the effect of chloride channels and MAPK signal pathway in the pathological process of hypoxia hypercapnia-induced pulmonary vasoconstriction 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 II persistent vasoconstrictive peak were significantly attenuated and then turn to vasodilatation compared with the HD group(P0.05 and P0.01) but the Phase I acute vasoconstriction and the Phase I vasodilation had no changes compared with HD(P0.05); The second pulmonary artery rings incubated by NFA+SB group who's vasoconstrictive peak was significantly attenuated compared with the NFA group(P0.05), but the NFA+U group didn抰 change(P0.05). Conclusion: Chloride channel blocker can inhibit MAPK signaling pathway, reduces the second branch pulmonary artery rings phase II sustained contraction, and reversed diastolic state, so as to play the role of HHPV antagonists.