中文摘要：

目的探讨硫化氢（H2S）在大鼠大脑中动脉（MCA）上是否具有内皮源性超极化因子（EDHF）样作用。方法应用离体血管舒缩功能测定方法,检测乙酰胆碱（ACh）、硫氢化钠（NaHS）等对大鼠离体MCA的舒张作用。血管用一氧化氮（NO）合酶抑制剂（L-NAME,3×10-5mol/L）和前列环素（PGI2）合酶抑制剂（Indo,1×10-5mol/L）预处理后,用ACh诱导血管产生非NO、非PGI2舒张反应。并观察四乙胺（TEA,1×10-3mol/L）或DL-炔丙基甘氨酸（PPG,1×10-4mol/L）对这种非NO、非PGI2舒张反应的影响。结果在30 mmol/L KCl预收缩的大鼠MCA上,ACh（10-7～10-4.5mol/L）和NaHS（10-5～10-2.5mol/L,H2S供体）均可浓度依赖性舒张大鼠MCA。血管用L-NAME（3×10-5mol/L）和Indo（1×10-5mol/L）预处理后,ACh对MCA仍具有明显的舒张作用（P〈0.01）。在1×10-3mol/L浓度时具有阻断钙激活钾通道作用的TEA或内源性H2S合成酶——胱硫醚-γ-裂解酶（CSE）的抑制剂PPG（1×10-4mol/L）均可明显取消ACh诱导大鼠MCA的这种非NO、非PGI2介导的舒张。结论在大鼠MCA中,ACh诱导的非NO、非PGI2舒张反应,即EDHF反应可能是H2S介导的。

英文摘要：

Objective To study whether hydrogen sulfide（H2S） induced the endothelium-derived hyperpolarizing factor（EDHF） dilation in rat middle cerebral artery（MCA） or not.Methods The relaxant effects of acetylcholine（ACh）,sodium hydrosulfide（NaHS） on isolated rat MCAs were detected by vasomotoricity experiment in vitro,respectively.Non-NO,non-PGI2 relaxation was induced by ACh in the presence of Nω-nitro-L-arginine-methyl-ester（L-NAME） and indomethacin（Indo）.The effects of tetraethylammonium（TEA,1×10-3 mol/L） or DL-propargylglycine（PPG,1×10-4 mol/L） on the non-NO,non-PGI2 relaxation were also observed.Results In the isolated rat MCAs preconstricted by 30 mmol/L KCl,ACh（10-7～10-4.5 mol/L） and NaHS（10-5～10-2.5 mol/L,a donor of H2S） had the concentration-dependent relaxation.The ACh-induced vasorelaxation was partly inhibited in the presence of 3×10-5 mol/L L-NAME and 1×10-5 mol/L Indo,but the left relaxation was still significant.ACh-induced vasorelaxation in the presence of L-NAME and Indo was almost abolished by TEA（an inhibitor of calcium-activated K＋ channels at 1×10-3 mol/L） or 1×10-4 mol/L PPG（an inhibitor of endogenous synthesis of H2S）.Conclusion In the rat MCA,ACh-induced non-NO,non-PGI2 relaxation,the so-called EDHF dilation might be mediated by H2S.