从人类末期失败的心脏中分离的腹腔细胞中延迟脱极化后的离子机制
A O Verkerk1, M W Veldkamp, A Baartscheer
1Department of Physiology, Experimental and Molecular Cardiology Group, Academic Medical Center, University of Amsterdam, The Netherlands. a.o.verkerk@amc.uva.nl
Circulation
|November 28, 2001
概括
在患有心力衰竭的人类心脏中,短暂的内向电流 (I(ti)) 和延迟后去极化 (DADs) 仅由-交换电流 (I(Na/Ca) 驱动,而不是激活的化物电流 (I(Cl(Ca))).
科学领域:
- 心脏病学 心脏病学
- 电子生理学 电子生理学
- 分子心脏病学分子心脏病学
背景情况:
- 动物模型表明,Ca2+激活的Cl2−电流 (I) 和Na2+/Ca2+交换电流 (I) 都有助于短暂的向内电流 (I).
- ) 涉及到前节律失常的延迟后分极化 (DADs).
- 人类心脏中I{}ti和DADs的精确离子机制仍然不完全理解.
研究的目的:
- 调查人类心室细胞中潜在的I (ti) 和DADs的特定离子机制.
- 确定人心衰竭细胞中I ((Cl ((Ca)) 和I ((Na/Ca)) 对I ((ti)) 和DADs的相对贡献.
主要方法:
- 人类心室细胞从末期心力衰竭患者的心脏中分离出来.
- 使用补丁方法来记录离子电流.
- 在特定的药理和离子条件下引起了I(ti) 和DADs,包括阻断I(Cl(Ca)) 和操纵细胞外Na(+).
主要成果:
- 电流被向内导向,跨越广泛的电压范围 (-110到+50mV).
- 无论是Cl-) 通道阻断剂,还是改变的细胞内Cl-) 度都没有影响I(ti) 或DAD振幅,排除了I(Cl(Ca)) 的重要作用.
- 通过用Li(+) 替换细胞外Na(+) 来阻断Na(+) /Ca(2+) 交换,观察到完全抑制I(ti).
结论:
- 在患有心脏衰竭的人类腹腔细胞中,I(ti) 和DADs完全由Na(+) /Ca(2+) 交换电流 (I(Na/Ca)) 介导.
- 这与许多动物物种的发现形成鲜明对比.
- 结果表明,在非失败的人类心室细胞中,在DADs期间I ((Cl ((Ca)) 也可能缺席.
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