格列本脲和亚甲蓝对缺氧诱发离体猪冠脉—过性舒张的影响  

Effects of glibenclamide and methylthioninium chloride on anoxia-induced transient relaxation of the isolated porcine coronary artery

作　　者：杨小平[1] 李蕴山[1] 傅绍萱[1] 

机构地区：[1]河北医学院药理教研室,石家庄050017

出　　处：《中国药理学与毒理学杂志》1992年第4期275-277,共3页Chinese Journal of Pharmacology and Toxicology

摘　　要：缺氧可诱发KC1 25 mmol·L^(-1)预收缩离体猪冠脉产生双相反应,先短暂(持续4.3±s0.8 min)舒张,随后持续收缩;除去内皮可消除缺氧诱发的冠脉舒张反应,并几乎完全消除收缩反应,格列本脲0.1,0.5,2.5和亚甲蓝5,10μmol·L^(-1)均可浓度依赖地抑制缺氧诱发的冠脉舒张反应;格列本脲2.5和亚甲蓝10μmol·L^(-1)合用可几乎完全消除此种舒张反应,提示缺氧诱发离体猪冠脉一过性舒张可能由ATP敏感性钾通道和内皮舒张因子(EDRF)共同中介。Anoxia caused a transient relaxation lasting 4.3± s 0.8 min, followed by a sustained contraction in the isolated porcine coronary artery stimulated by KC1 25 mmol·L; the removal of the endothelium abolished the anoxia induced relaxation of the coronary artery, and almost eliminated the contraction response. Glibenclamide (Gli) 0.1, 0.5, 2.5 and methylthioninium chloride (MC) 5, 10 μmol·L-1 produced a concentration-dependent decrease in the relaxation response of the coronary artery caused by anoxia, and a combination of Gli 2.5 and MC 10μmol·L-1 almost abolished the dilation. These data indicate that anoxia-induced transient relaxation of the isolated porcine coronary artery possibly is mediated by the combined effects of the ATP-sensitive potassium channel and the endothelium-derived relaxing factor (EDRF).

关 键 词：格列本脲 亚甲蓝 冠状血管缺氧 

分 类 号：R965[医药卫生—药理学]