映山红花总黄酮对全脑缺血再灌注大鼠脑基底动脉超极化反应的诱导作用  

Inducing effect of total flavones in rhododendra on endothelium-derived hyperpolarizing factor responses in cerebral basilar artery of rats subjected to global cerebral ischemia reperfusion

作　　者：韩黎黎[1] 范一菲[1] 陈志武[1] 

机构地区：[1]安徽医科大学基础医学院药理教研室,安徽合肥230032

出　　处：《中草药》2011年第6期1164-1168,共5页Chinese Traditional and Herbal Drugs

基　　金：国家自然科学基金资助项目(30840104);高等学校博士点专项科研基金资助项目(2007036605)

摘　　要：目的探讨映山红花总黄酮(TFR)对内皮源性超极化因子(EDHF)介导的全脑缺血再灌注大鼠脑基底动脉(CBA)血管舒张和平滑肌细胞膜静息电位超极化反应的诱导作用。方法采用四血管结扎法建立大鼠全脑缺血再灌注模型,测定离体大鼠CBA平滑肌细胞膜静息电位和血管舒张功能。结果在3×10-5 mol/L L–NAME和1×10-5 mol/L吲哚美辛存在时,全脑缺血再灌注可明显促进乙酰胆碱(Ach,1×10-7～1×10-5 mol/L)诱导大鼠CBA产生非NO、非PGI2介导的血管舒张和平滑肌细胞膜静息电位超极化;TFR 11～2 700 mg/L可使全脑缺血再灌注大鼠CBA产生较明显的非NO、非PGI2介导的血管舒张和平滑肌细胞膜静息电位超极化反应,并能被Ca2+激活的K通道阻断剂四乙胺(TEA,1 mmol/L)和内源性硫化氢(H2S)生成抑制剂dl-炔丙基甘氨酸(PPG,1×10-4 mol/L)显著抑制。结论全脑缺血再灌注明显增强大鼠CBA中非NO、非PGI2介导的血管舒张和平滑肌细胞超级化。TFR明显诱导全脑缺血再灌注大鼠CBA产生此种血管舒张和超级化,即EDHF反应,并可能与H2S有关。Objective To study the effect of endothelium-derived hyperpolarizing factor（EDHF）-mediated responses of relaxation and hyperpolarization of vascular smooth muscle cell（VSMC） of rat cerebral basilar artery（CBA） subjected to cerebral ischemia/reperfusion（I/R） to total flavones in rhododendra（TFR）.Methods The model of global cerebral I/R in rats was made by 4-vessel occlusion（4-VO）.The vasodilation and resting membrane potential（RMP） of VSMC of rat CBA were detected in vitro.Results In the presence of 3×10？5 mol/L Nω-nitro-L-arginine-methyl-ester（L-NAME,an inhibitor of nitric oxide synthase） and 1×10？5 mol/L Indomethacin（Indo,an inhibitor of PGI2 synthesis）,the global cerebral I/R markedly enhanced 1×10？7-1×10？5 mol/L acetylcholine（Ach）-elicited relaxation and hyperpolarization of RMP of VSMC in rat CBA.In the presence of L–NAME and Indo,11-2 700 mg/L TFR induced significant and dose-dependent hyperpolarization of RMP of VSMC and relaxation of rat CBA subjected to global cerebral I/R.The hyperpolarization and relaxation were obviously inhibited by tetraethylammonium（an inhibitor of IKCa at 1 mmol/L） and 1×10？4 mol/L dl-propargylglycine（PPG）,an inhibitor of endogenous hydrogen sulfide（H2S） synthase.Conclusion Global cerebral I/R could enhance the non-NO-non-PGI2-mediated responses of hyperpolarization and vasorelaxation in rat CAB.In rat CAB subjected to global cerebral I/R,TFR could significantly induce this non-NO-non-PGI2 hyperpolarization and relaxation,the so-called EDHF response that might be mediated by endogenous H2S.

关 键 词：映山红 总黄酮 内皮源性超极化因子 硫化氢 血管舒张 超极化反应 

分 类 号：R285.5[医药卫生—中药学]