中文摘要：

碘化N-正丁基氟哌啶醇（N-n-butyl haloperidol iodide,F2）为本研究室改造合成的新化合物.前期研究发现F2作为L-型钙通道拮抗剂,能剂量依赖地拮抗缺血再灌注所导致的大鼠心脏损伤.研究F2对缺氧复氧（hypoxia/reoxygenation,H/R）大鼠心肌细胞钠钙交换体电流的作用并探讨其保护机制.采用Langendorff灌流系统灌流SD大鼠心脏,标准酶解法消化分离得到单个心室肌细胞.正常台式液灌流5 min,立即灌流充90％N2-10％CO2的缺氧液,建立体外心肌细胞H/R模型,采用全细胞膜片钳技术记录对照、模型以及不同浓度F2（0.1、1、10 μmol/L）对心肌细胞钠钙交换体电流,观察H/R状态F2对心肌细胞钠钙交换体电流的影响.结果显示：缺氧抑制钠钙交换体电流主要是抑制外向电流;H/R引起钠钙交换体电流增大,尤其是外向电流的增大.F2呈浓度依赖地抑制钠钙交换体电流,钠钙交换体电流I-V曲线上移.以上表明：F2能抑制钠钙交换体电流,尤其是外向电流,防止H/R时心肌细胞的钙超载,保护心肌细胞.

英文摘要：

The study was designed to investigate the effects of N n butyl haloperidol iodide （F2） on sodium/calcium exchanger currents （NCX） including outward and inward currents during hypoxia/reoxygenation （H/R） in rat ventricular myocytes. Single ventricular cells were obtained by enzymatic dissociation. In whole-cell patch clamp studies, the NCX outward and inward cur- rents （INcx） were recorded from isolated rat ventricular myocytes. Results show that hypoxia inhibited the INcx, especially the outward current. H/R enhanced the amplitude of INcx obviously, especially the outward current. F2 inhibited INcx in a concentra tion-dependent manner,especially the outward current. Our study suggests that Fe can protect myocytes from H/R injury, which might be related to the inhibition of the inward and outward of INcx.