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首页> 外文期刊>Cellular Physiology and Biochemistry >N-n-butyl haloperidol iodide preserves cardiomyocyte calcium homeostasis during hypoxia/ischemia
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N-n-butyl haloperidol iodide preserves cardiomyocyte calcium homeostasis during hypoxia/ischemia

机译：N-正丁基氟哌啶醇碘化物可在缺氧/缺血期间保持心肌细胞钙稳态

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Aims: N-n-Butyl haloperidol iodide (F_2) is a novel compound derived from haloperidol. In our previous work, F_2 was found to be an L-type calcium channel blocker which played a protective role in rat heart ischemic-reperfusion injury in a dose-dependent manner. In the current study, we aimed to investigate the effects and some possible mechanisms of F_2 on calcium transients in hypoxic/ischemic rat cardiac myocytes. Methods and Results: Calcium transients' images of rat cardiac myocytes were recorded during simulated hypoxia, using a confocal calcium imaging system. The amplitude, rising time from 25% to 75% (RT25-75), decay time from 75% to 25% (DT75-25) of calcium transients, and resting [Ca~(2+)]_i were extracted from the images by self-coding programs. In this study, hypoxia produced a substantial increase in diastolic [Ca~(2+)]_i and reduced the amplitude of calcium transients. Both RT25-75 and DT75-25 of Ca~(2+) transients were significantly prolonged. And F_2 could reduce the increase in resting [Ca~(2+)]_iand the prolongation of RT25-75 and DT75-25 of Ca~(2+) transients during hypoxia. F_2 also inhibited the reduction in amplitude of calcium transients which was caused by 30-min hypoxia. The activity of SERCA2a (sarcoplasmic reticulum Ca ~(2+)-ATPase, determined by test kits) decreased after 30-min ischemia, and intravenous F_2 in rats could ameliorate the decreased activity of SERCA2a. The inward and outward currents of NCX (recorded by whole-cell patch-clamp analysis) were reduced during 10-min hypoxia, and F_2 further inhibited the outward currents of NCX during 10-min hypoxia. All these data of SERCA2a and NCX might be responsible for the changes in calcium transients during hypoxia. Conclusion: Our data suggest that F_2 reduced changes in calcium transients that caused by hypoxia/ischemia, which was regarded to be a protective role in calcium homeostasis of ventricular myocytes, probably via changing the function of SERCA2a.
机译：目的：正丁基碘氟哌啶醇碘化物（F_2）是一种衍生自氟哌啶醇的新型化合物。在我们以前的工作中，发现F_2是一种L型钙通道阻滞剂，它以剂量依赖的方式在大鼠心脏缺血再灌注损伤中起保护作用。在当前的研究中，我们旨在研究F_2对缺氧/缺血大鼠心肌细胞钙瞬变的影响及其可能的机制。方法和结果：使用共聚焦钙成像系统在模拟的缺氧期间记录大鼠心肌细胞的钙瞬变图像。从图像中提取了钙瞬变的幅度，上升时间从25％到75％（RT25-75），衰减时间从75％到25％（DT75-25）和静止的[Ca〜（2 +）] _ i。通过自编码程序。在这项研究中，缺氧导致舒张期[Ca〜（2 +）] _ i大量增加，并降低了钙瞬变的幅度。 Ca〜（2+）瞬变的RT25-75和DT75-25均显着延长。 F_2可以减少[Ca〜（2+）]静息的增加，并降低缺氧时Ca〜（2+）瞬态的RT25-75和DT75-25的延长。 F_2还抑制了30分钟缺氧引起的钙瞬变幅度的降低。缺血30分钟后，SERCA2a的活性（肌浆网Ca〜（2 +）-ATPase，由试剂盒测定）降低，并且大鼠静脉内F_2可以减轻SERCA2a活性的降低。在缺氧10分钟时，NCX的内向和外向电流（通过全细胞膜片钳分析记录）降低，而F_2在缺氧10分钟内进一步抑制NCX的外向电流。 SERCA2a和NCX的所有这些数据可能与缺氧期间钙瞬变的变化有关。结论：我们的数据表明F_2减少了由缺氧/缺血引起的钙瞬变变化，这可能是通过改变SERCA2a的功能来保护心室肌钙稳态。

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