...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Electrophysiological Effects of Lysophosphatidylcholine on HL-1 Cardiomyocytes Assessed with a Microelectrode Array System
【24h】

Electrophysiological Effects of Lysophosphatidylcholine on HL-1 Cardiomyocytes Assessed with a Microelectrode Array System

机译：微电极阵列系统评估溶血磷脂酰胆碱对HL-1心肌细胞的电生理作用

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

biBackground /i/bSudden death due to malignant ventricular arrhythmias is the most important cause of death in acute myocardial infarction. Improved knowledge about the pathophysiology underlying these arrhythmias is essential in the search for new anti-arrhythmic strategies. Lysophosphatidylcholine (LPC), a hydrolysis product of (membrane) phospholipid degradation, is one of the most potent pro-arrhythmic substances that accumulate in the human heart during myocardial ischemia. The aim of this study was to set up and validate an iin vitro /iexperimental system for studies on the effects of LPC on electrophysiological parameters in beating cardiomyocytes. biMethods and Results /i/bSpontaneously beating HL-1 cardiomyocytes were cultured on multielectrode array microchips for three days for the recording of electrical activities in the form of field potentials (FP). FPs were recorded at baseline and after addition of 2, 4, 8, 12, 16, 20, and 24 µM of LPC to the cell medium (n=9). We found that LPC could induce rapid effects on electrical parameters in the HL-1 cells. The overall half-maximal effective concentration (ECsub50/sub) of LPC was around 12 µM. The beating rate and peak-peak amplitude of FP thus decreased at concentrations ≥ 12 µM and were inversely proportional to increased LPC concentration. The duration of FP was significantly prolonged with LPC above 12 µM and was concentration-dependent. LPC delayed signal propagation, an effect which was mimicked by blocking gap junctions with heptanol and attenuated by pre-treatment with isoprenaline and atropine. Finally, asynchronous activity was induced by LPC at 12 µM. biConclusions /i/bLPC induced prompt and pronounced electrophysiological alterations that may underlie its observed pro-arrhythmic properties. Our iin vitro /imodel with HL-1 cells and microelectrode array system may be a useful tool for preclinical studies of electrophysiological effects of various pathophysiological concepts.
机译：背景 恶性室性心律失常导致的猝死是急性心肌梗死的最重要死因。在寻找新的抗心律不齐策略时，对这些心律失常的病理生理学知识的深入了解至关重要。溶血磷脂酰胆碱（LPC）是（膜）磷脂降解的水解产物，是在心肌缺血期间在人心脏中积累的最有效的心律失常物质之一。这项研究的目的是建立和验证用于研究LPC对跳动的心肌细胞电生理参数影响的体外实验系统。 方法和结果 自发跳动的HL-1心肌细胞在多电极阵列微芯片上培养三天，以电场电位（FP）的形式记录电活动。在基线时以及向细胞培养基中添加2、4、8、12、16、20和24 µM LPC之后记录FP（n = 9）。我们发现LPC可以诱导HL-1细胞中的电参数快速影响。 LPC的总半数最大有效浓度（EC 50 ）约为12 µM。因此，在浓度≥12 µM时，FP的跳动速率和峰峰幅度降低，并且与LPC浓度升高成反比。 LPC高于12 µM时，FP的持续时间显着延长，并且是浓度依赖性的。 LPC延迟了信号的传播，这种效果可以通过用庚醇阻断缝隙连接来模仿，而通过用异丙肾上腺素和阿托品进行预处理可以减弱。最后，> 12 µM的LPC诱导了异步活动。 结论 LPC引起迅速而明显的电生理改变，可能是其观察到的心律失常特性的基础。我们的带有HL-1细胞和微电极阵列系统的体外模型可能是临床前研究各种病理生理学概念的电生理作用的有用工具。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号