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J Am Coll Cardiol, 2007; 50:626-633, doi:10.1016/j.jacc.2007.03.060 (Published online 29 July 2007).
© 2007 by the American College of Cardiology Foundation
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Central Sympatholysis as a Novel Countermeasure for Cocaine-Induced Sympathetic Activation and Vasoconstriction in Humans

Dileep V. Menon, MD, Zhongyun Wang, MD, Paul J. Fadel, PhD, Debbie Arbique, RN, David Leonard, PhD, Jia-Ling Li, MD, Ronald G. Victor, MD, FACC1 and Wanpen Vongpatanasin, MD, FACC1,*

Hypertension Division and the Donald W. Reynolds Cardiovascular Clinical Research Center, University of Texas Southwestern Medical Center, Dallas, Texas.


Figure 1
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  		Figure 1 Original Recordings of Skin SNA

Intranasal cocaine evoked a rapid and sustained increase in skin sympathetic nerve activity (SNA), which is reversed by dexmedetomidine (Dex), beginning at the dose of 0.1 µg/kg/min but not by intravenous saline. The SNA is in arbitrary units along the Y-axis.

 

Figure 2
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  		Figure 2 Changes in Skin SNA and Skin Vascular Resistance In Response to Cocaine and Dex

Intranasal cocaine increased skin sympathetic nerve activity (SNA), which was accompanied by a parallel increase in skin vascular resistance. Dexmedetomidine (Dex) reversed effects of cocaine on SNA and skin vascular resistance, beginning at the dose of 0.1 µg/kg/min. Data are mean ± SE. *p < 0.05 versus baseline, {dagger}p < 0.01 versus baseline, {ddagger}p < 0.05 versus saline, §p < 0.01 versus saline.

 

Figure 3
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  		Figure 3 Changes in Skin SNA and Vascular Resistance in Subjects With {alpha}2CDel322-325 Allele

Intranasal cocaine caused a similar increase in skin sympathetic nerve activity (SNA) and skin vascular resistance in both groups of subjects. Dexmedetomidine (Dex) reversed effects of cocaine on SNA and skin vascular resistance similarly in both groups. Data are mean ± SE. *p < 0.05 versus baseline, {dagger}p < 0.01 versus baseline.

 




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Copyright © 2007 by the American College of Cardiology Foundation.