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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。
Hypoxia induced a biphasic response to precontracted porcine coronary arteries (KC1 25 mmol·L -1) for a short period of time (lasting 4.3 ± 0.8 min) and then continued to contract; removal of endothelium abolished hypoxia-induced Of coronary diastolic response and almost completely eliminate the contractile response, glibenclamide 0.1,0.5,2.5 and methylene blue 5,10μmol·L -1 concentration-dependent inhibition of hypoxia-induced coronary vasodilation ; Glibenclamide 2.5 and methylene blue 10μmol·L -1 can almost completely eliminate this diastolic reaction, suggesting that transient hypoxia-induced porcine coronary diastole may be caused by the ATP-sensitive potassium channels and endothelial Relaxation factor (EDRF) common intermediary.