加多降低了拉伸引起的对心房动的脆弱性
F Bode1, A Katchman, R L Woosley
1Department of Pharmacology, Georgetown University, Veterans Affairs Medical Center, Washington, DC 20422, USA.
Circulation
|May 10, 2000
概括
心房拉伸增加了心房动 (AF) 的风险. 用加多 (Gd3+) 阻断拉伸激活通道 (SAC) 显著降低了这种脆弱性,这表明了AF的新抗失常策略.
科学领域:
- 心脏病学 心脏病学
- 电子生理学 电子生理学
- 药理学 药理学是指药理学的学科.
背景情况:
- 心房动 (AF) 与由压力/体积过载引起的心房扩大有关.
- 心肌细胞中的拉伸激活通道 (SAC) 可能会在扩张的心房中导致AF.
研究的目的:
- 为了研究SAC阻塞物加多 (Gd3+) 在隔离的子心脏中在心房拉伸期间对AF倾向的影响.
主要方法:
- 使用了隔离的兰登多夫透的子心脏.
- 心房压升高,并通过爆发节奏评估AF脆弱性.
- 加多 (Gd3+) 用于增加剂量 (12.5,25,50μmol/L).
主要成果:
- 在Gd3+给药后,AF诱导需要显著提高心房压力 (19.0±0.5厘米H2O与50μmol/LGd3+相比,8.8±0.2厘米H2O基线).
- 剂量取决于Gd3+降低了AF脆弱性,并防止了自发的AF运行.
- Gd3+没有显著影响心房有效耐火期.
结论:
- 急性心房拉伸增强了AF的脆弱性.
- 加多 (Gd3+) 有效地以剂量依赖的方式减少拉伸诱导的AF脆弱性.
- 阻断SAC可能为AF提供一种与心房压力或体积升高相关的新型抗心律失常方法.
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