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作 者:杨小平[1] 武占军[1] 许彦芳[1] 董伟 杨伟 傅绍萱[1] 李蕴山[1]
机构地区:[1]河北医学院药理教研室
出 处:《中国药理学报》1994年第4期323-326,共4页Acta Pharmacologica Sinica
基 金:Natural Science Foundation of Hebei Province.№ 393126.
摘 要:左旋硝基精氨酸,NLA (0.2 mmol·L^(-1))可阻断离体猪冠脉依内皮性缺氧收缩反应,用左旋精氨酸,L-Arg(2mmol·L^(-1))预处理可显著降低NLA的抑制作用,四乙胺,TEA(10mmol·L^(-1))和格列本脲,Gli(1 μmol·L^(-1))对缺氧收缩反应无明显影响,而Cro-makalim,Cro(1 μmol·L^(-1))则可抑制缺氧冠脉收缩。Exposure of isolated pig coronary artery with endothelium intact to hypoxia Krebs-Henseleit solution aerated with 95 % N2 + 5 % CO2 caused a transient. contractile response , and the coronary artery without endothelium exhibited a gradual decrease in basal tension. The endothelium-dependent contractile response to hypoxia was almost completely blocked by nitro-L-arginine (0. 2 mmol·L-1) , and inhibited by methylthioni-nium chloride (10 μmol·L-1). The inhibitory effect of the NLA was partially reversed by L-arginine (2 mmol·L-1). Sodium nitroprus-side (10 μmol· L-1) was also completely antagonized and nicorandil (0.3 mol·L-1) remarkably reduced the hypoxic contractile response. Tetraethylammonium (10 mmol ·L-1) and glibenclamide (1 μmol·L-1) had little effect on hypoxia-induced vascular con-straction, whereas cromakalim (1 μmol·L-1) produced obvious relaxing effect on hypoxic response. These results suggest that suppression of basally released nitric oxide (NO) is an important mechanism of coronary vaso-constriction induced by hypoxia.
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