激活的Cl ((-) 电流有助于延迟单个普尔金耶和心室肌细胞的脱极化后
A O Verkerk1, M W Veldkamp, L N Bouman
1Department of Physiology, Academic Medical Center, University of Amsterdam, The Netherlands. a.o.verkerk@amc.uva.nl
Circulation
|June 7, 2000
概括
心脏细胞中的短暂向内流 (I(ti)) 涉及 (Cl-) 和 (Na+-Ca2+) 交换电流. 阻止Cl-电流成分可能有助于通过减少延迟脱极化后 (DADs) 来预防心律失常.
科学领域:
- 心脏电生理学 心脏电生理学
- 离子通道生理学 离子通道生理学
- 心血管药理学心血管药理学
背景情况:
- 短暂的向内电流 (I(ti)) 是延迟后分极化 (DADs) 的基础,这是心律失常的关键因素.
- 在心室肌细胞和普金尼纤维之间,I(ti) 的离子机制不同,之前的研究涉及Na+-Ca2+交换,Cl-电流和非选择性离子电流.
研究的目的:
- 为了阐明一只羊Purkinje和心室肌细胞中的I ((ti) 的离子基.
- 为了研究阻断I(ti) 的Cl-电流成分的抗节律障碍潜力.
主要方法:
- 整个细胞补丁电生理学被用于孤立的羊Purkinje和心室肌细胞.
- 在诺拉上腺素的存在下,使用重复的脱极化诱导了I(ti).
- 评估了离子阻断剂4,4'-二二基亚诺乙烯-2,2'-二硫酸 (DIDS) 和Na+-Ca2+交换阻断的作用.
主要成果:
- 在两种细胞类型中,呈现了负电位的进流和正电位的外流.
- DIDS完全阻断了外向组件,并略微抑制了I(ti) 的内向组件.
- 对DIDS敏感的I(ti) 组件是外观纠正,与Cl-电流一致,而对DIDS不敏感的组件则被Na+-Ca2+交换封锁取消.
结论:
- 在普尔金耶细胞和腹腔肌细胞中,I (ti) 通过两个不同的离子机制进行介导:Cl-电流和Na+-Ca2+交换电流.
- 阻断I(ti) 的Cl-电流成分显著降低了DAD振幅和触发活动,这表明潜在的抗不律性益处.
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