[关键词]
[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。
[Key word]
[Abstract]
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.
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[基金项目]
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）
