AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 294: H605-H612, 2008. First published November 30, 2007; doi:10.1152/ajpheart.01162.2007
0363-6135/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
294/2/H605    most recent
01162.2007v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Spaak, J.
Right arrow Articles by Floras, J. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Spaak, J.
Right arrow Articles by Floras, J. S.

Dose-related effects of red wine and alcohol on hemodynamics, sympathetic nerve activity, and arterial diameter

Jonas Spaak,1 Anthony C. Merlocco,1 George J. Soleas,2 George Tomlinson,1 Beverley L. Morris,1 Peter Picton,1 Catherine F. Notarius,1 Christopher T. Chan,1 and John S. Floras1

1University Health Network and Mount Sinai Hospital Division of Cardiology, Department of Medicine, University of Toronto; and 2Quality Assurance Laboratory, Liquor Control Board of Ontario, Toronto, Ontario, Canada

Submitted 8 October 2007 ; accepted in final form 27 November 2007

The cardiovascular benefits of light to moderate red wine consumption often have been attributed to its polyphenol constituents. However, the acute dose-related hemodynamic, vasodilator, and sympathetic neural effects of ethanol and red wine have not been characterized and compared in the same individual. We sought to test the hypotheses that responses to one and two alcoholic drinks differ and that red wine with high polyphenol content elicits a greater effect than ethanol alone. Thirteen volunteers (24–47 yr; 7 men, 6 women) drank wine, ethanol, and water in a randomized, single-blind trial on three occasions 2 wk apart. One drink of wine and ethanol increased blood alcohol to 38 ± 2 and 39 ± 2 mg/dl, respectively, and two drinks to 72 ± 4 and 83 ± 3 mg/dl, respectively. Wine quadrupled plasma resveratrol (P < 0.001) and increased catechin (P < 0.03). No intervention affected blood pressure. One drink had no heart rate effect, but two drinks of wine increased heart rate by 5.7 ± 1.6 beats/min; P < 0.001). Cardiac output fell 0.8 ± 0.3 l/min after one drink of ethanol and wine (both P < 0.02) but increased after two drinks of ethanol (+0.8 ± 0.3 l/min) and wine (+1.2 ± 0.3 l/min) (P < 0.01). One alcoholic drink did not alter muscle sympathetic nerve activity (MSNA), while two drinks increased MSNA by 9–10 bursts/min (P < 0.001). Brachial artery diameter increased after both one and two alcoholic drinks (P < 0.001). No beverage augmented, and the second wine dose attenuated (P = 0.02), flow-mediated vasodilation. One drink of ethanol dilates the brachial artery without activating sympathetic outflow, whereas two drinks increase MSNA, heart rate, and cardiac output. These acute effects, which exhibit a narrow dose response, are not modified by red wine polyphenols.

microneurography; sympathetic nervous system; blood pressure; cardiovascular diseases; risk factors



Address for reprint requests and other correspondence: J. Spaak, Dept. of Clinical Sciences, Section of Cardiology, Karolinska Institutet at Danderyd Univ. Hospital, 182 88 Stockholm, Sweden (e-mail: jonas.spaak{at}ds.se)




This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
T. Lahm, P. R. Crisostomo, T. A. Markel, M. Wang, Y. Wang, J. Tan, and D. R. Meldrum
Selective estrogen receptor-{alpha} and estrogen receptor-{beta} agonists rapidly decrease pulmonary artery vasoconstriction by a nitric oxide-dependent mechanism
Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2008; 295(5): R1486 - R1493.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.