Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation
Michel L. Hijmering, MD*,
Erik S. G. Stroes, MD, PhD ,*,
Jobien Olijhoek, MD ,
Barbara A. Hutten, MSc, PhD ,
Peter J. Blankestijn, MD, PhD|| and
Ton J. Rabelink, MD, PhD
* Department of Internal Medicine, Eemland Hospital, Amersfoort, The Netherlands
Vascular Medicine, Eemland Hospital, Amersfoort, The Netherlands
Clinical Epidemiology and Biostatistics, Academic Medical Centre, Amsterdam, The Netherlands
Internal Medicine, University Medical Center, Utrecht, The Netherlands
|| Department of Nephrology, University Medical Center, Utrecht, The Netherlands
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Figure 1 Effect of lower body negative pressure (LBNP) on flow-mediated dilation. Flow-mediated dilation decreased significantly during LBNP (–20 mm Hg) in healthy volunteers (*p = 0.0008 by the paired t test). Bold line = average value of all observations.
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Figure 2 Effect of lower body negative pressure (LBNP) on reactive hyperemic flow and heart rate. (A, left) Basal and maximal post-ischemic flow at baseline. (A, right) Basal flow and maximal post-ischemic flow during LBNP. The increase in blood flow during hyperemia was not significantly different between baseline and LBNP (p = 0.099 by two-way repeated measures analysis of variance). (B) Lower body negative pressure significantly increased the heart rate (*p = 0.0013 by the paired t test).
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Figure 3 Effect of alpha-receptor blockade on the flow-mediated dilation (FMD)/nitroglycerin (NTG) response with and without lower body negative pressure (LBNP). (A) During phentolamine (PE) (solid squares), the LBNP-induced impairment in FMD (solid circles) could no longer be demonstrated (two-way repeated measures analysis of variance: *p = 0.046 control vs. PE). (B) Phentolamine (solid squares) did not change the NTG response compared with baseline (solid circles) (p = NS).
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