可卡因通过一个中心作用机制刺激人类的心血管系统
W Vongpatanasin1, Y Mansour, B Chavoshan
1Divisions of Hypertension and Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Circulation
|August 3, 1999
概括
在人类中,可卡因显著增加了中心交感神经活动 (SNA),导致血管收缩和心率增加. 这项研究提供了可卡因的直接证据.
科学领域:
- 心血管生理学心血管生理学
- 神经药理学神经药理学
- 人体生理学 人体生理学
背景情况:
- 可卡因对心血管的影响部分归因于阻断北上腺素的再吸收.
- 以前的理解并没有完全阐明可卡因对中心交感和副交感外流的影响.
研究的目的:
- 调查可卡因是否通过增加中央同情力外流来刺激人类心血管系统.
- 为了确定可卡因是否会降低心率的副交感控制.
主要方法:
- 微神经图被用来测量皮肤交感神经活动 (SNA) 在健康,可卡因素朴的人类.
- 血压,心率和皮肤血流在注射内鼻可卡因或利多卡因之前,期间和之后被监测.
- 药理阻塞 (propranolol, atropine) 用于评估可卡因对心率的影响的调解.
主要成果:
- 鼻腔内可卡因导致皮肤SNA显著持续增加,长达90分钟.
- 可卡因的使用导致皮肤血流减少,血管抵抗增加,心率升高.
- 可卡因诱导的心动减速被β-上腺体阻塞消除,但不是由肌肉蛋白阻塞消除.
结论:
- 直接的微神经图证据证实,鼻腔内可卡因在人类中刺激了中心交感外流.
- 可卡因诱导的交感激活会影响皮肤循环 (血管收缩) 和心脏 (心跳骤停).
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