摘要
以往的研究已证明，一氧化氢、前列环素和ATP敏感K+通道均参与低氧性脑血管扩张作用，然而它们之间的相互作用关系尚不清楚，这是本研究的目的．研究用初生小牛基底动脉血管条，观察低氧下（灌流溶液的氢分压为6．0kPa．二氧化碳分任为4．7kPa，pH为7．40±0．02）一氧化氮与前列环素，前列环素与ATP敏感K+通道及ATP敏感K+通道与一氧化氮在脑血管扩张反应申的相互关系．实验结果发现，一氧化氮对前列环素的作用无明显影响．而一氧化氮的作用似乎有赖于前列环素的存在；前列环素对ATP敏感K+通道的活动影响不大，而前列环素对脑血管的作用可能有赖于ATP敏感K+通道；一氧化氮的作用可能不是直接借助于ATP敏感K+通道的作用，ATP敏感K+通道的抑制对一氧化氮也无明显的影响。上述结果提示．在三种扩血管因素中，唯有ATP敏感K+通道的开放所引起的扩血管反应设有受内皮细胞产生的一氧化氮和前列环素两个因子的明显影响，而其化两因子之间有相互的影响作用．
Aim Previous studies have demonstrated that ni- tric oxide (No) prostacyclin (PGI2) and ATP-sensi- tive K+ channel all participate in the regulation of hy- poxic cerebrovascular dilatation. but the interrelations of them still keep unclear. The aim of the study is to investigate the interrelations of these three vasodila- tive factors under hypoxia. Methods The experiments were Performed in new-born calf basilar arteral strips to observe the interrela-tions between NO and PGI:, Pt7[, and ATP-sensitive K+ channel, ATP-sensitive K channel and NO, re- spetively, in hypoxic cerebrovascular dilatation (the bypoxic Perfusion solation was prepared with PO2 6. 0 kPa, PCO2, 4. 7 kPa, and pH 7. 40±0. 02 ).Results The NO bad no effect of PGI2, but dilata-tion induced by NO appears to depend on production of PGI2, PGI2 had no obvious effect on ATP-sensitive K+ channel, but the effects of PGI2 may be dependent on openning of ATP-sensitive K - channel ; the effects of No may be not directely mediated by openning of ATP-sensitive K+ channel. and the activities of ATP- sensitive K+ channel seem isolated from effect of NO.Conclusions The response of hypoxic cerebrovas-cular dilatation are influenced obviously by No and PGI2 except reaction induced by ATP-sensitive K+ channel. There are some interrelative effects be-tween NO and PGI2, but the openning of ATP-sensi-tive K+ channel in not innuenced by them.
出处
《中国动脉硬化杂志》
CAS
CSCD
1997年第1期19-22,共4页
Chinese Journal of Arteriosclerosis
关键词
低氧
扩血管因子
脑血管
ypoxia
Vasodilative factor
Cerebrovessel
