摘要
目的:探索电压依赖性钾离子通道(K V)和p38丝裂原活化蛋白激酶(MAPK)信号通路在低氧高二氧化碳性肺血管收缩(HHPV)中的作用。方法:制作正常SD大鼠离体二级肺动脉环,在常氧及低氧高二氧化碳条件下观察肺动脉环的张力变化;在急性低氧高二氧化碳条件下,分别用K V阻断剂4-氨基吡啶(4-AP)、p38 MAPK信号通路抑制剂SB203580和4-AP+SB203580孵育二级肺动脉环,测定各组血管环的张力值。结果:在急性低氧高二氧化碳条件下,(1)肺动脉环呈现双相性的收缩(P<0.05或P<0.01);(2)经4-AP孵育的二级肺动脉环,II期收缩幅度增强(P<0.05或P<0.01);(3)SB203580能使4-AP所致的二级肺动脉环II期持续收缩幅度显著降低(P<0.05或P<0.01)。结论:4-AP可增强大鼠HHPV的作用,而SB203580能使4-AP所致的二级肺动脉环II期持续收缩幅度显著降低,提示p38 MAPK信号通路的参与可能是K V调节大鼠HHPV作用的重要机制之一。
AIM : To investigate the roles of voltage-dependent KV channel ( Kv ) and p38 mitogen-activated protein kinase (MAPK) signal pathway in the pathological process of hypoxia hypercapnia-induced pulmonary vasoconstric- tion (HHPV) in rats. METHODS: The second-order pulmonary artery rings isolated from SD rats in vitro was prepared, and randomly divided into control group (N group) , hypoxia hypercapnia group (H group), hypoxia hypercapnia + DMSO incubation group (HD group), hypoxia hypercapnia +4-aminopyridione (4-AP) group (4-AP group), hypoxia hypercap- nia + SB203580 incubation group (SB group) and hypoxia hypercapnia + 4-AP + SB203580 incubation group (4-AP + SB group). Under acute hypoxia hypercapnia condition, the changes of the 3 stages of HHPV incubated by 4-AP or the com- bined application of 4-AP and SB203580 were observed. At the same time, the tension values of the rings were recorded. RESULTS: Under hypoxia hypercapnia condition, a biphasic pulmonary artery contractile response was observed. The phase II persistent vasoconstriction of the pulmonary artery rings incubated with 4-AP was enhanced. Under hypoxia hyper- capnia condition, SB203580 significantly relieved the phase II persistent vasoconstriction induced by 4-AP. CONCLU- SION : The Kv blocker 4-AP enhances HHPV. SB203580 significantly relieves the phase II persistent vasoconstriction in- duced by 4-AP, indicating that the participation of p38 MAPK may be one of the important mechanisms for the regulation ofHHPV by Kv in the rats.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2013年第12期2268-2271,2276,共5页
Chinese Journal of Pathophysiology
基金
卫生部科学研究基金-浙江省医药卫生重大科技项目(No.WKJ2009-2-030)
浙江省中医药重点学科建设计划(No.2012-XK-A28)