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5min,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、10μmol/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。
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.
出处
《中国科技论文》
CAS
北大核心
2014年第3期370-374,共5页
China Sciencepaper
基金
高等学校博士学科点专项科研基金资助项目(200805600003)
国家自然科学基金资助项目(U0932005)
关键词
碘化N-正丁基氟哌啶醇
全细胞膜片钳
缺氧复氧
钠钙交换体电流
N-n-butyl haloperidol iodide
whole-cell patch-clamp techniques
hypoxia/reoxygenation
NCX outward and inward currents
