SYMPATHETIC WITHDRAWAL AND FOREARM VASODILATION DURING VASOVAGAL SYNCOPE IN HUMANS

Citation
Nm. Dietz et al., SYMPATHETIC WITHDRAWAL AND FOREARM VASODILATION DURING VASOVAGAL SYNCOPE IN HUMANS, Journal of applied physiology, 82(6), 1997, pp. 1785-1793
Citations number
39
Categorie Soggetti
Physiology,"Sport Sciences
ISSN journal
87507587
Volume
82
Issue
6
Year of publication
1997
Pages
1785 - 1793
Database
ISI
SICI code
8750-7587(1997)82:6<1785:SWAFVD>2.0.ZU;2-7
Abstract
Our aim was to determine whether sympathetic withdrawal alone can acco unt for the profound forearm vasodilation that occurs during syncope i n humans. We also determined whether either vasodilating beta(2)-adren ergic receptors or nitric oxide (NO) contributes to this dilation. For earm blood flow was measured bilaterally in healthy volunteers (n = 10 ) by using plethysmography during two bouts of graded lower body negat ive pressure (LBNP) to syncope. In one forearm, drugs were infused via a brachial artery catheter while the other forearm served as a contro l. In the control arm, forearm vascular resistance (FVR) increased fro m 77 +/- 7 units at baseline to 191 +/- 36 units with -40 mmHg of LBNP (P < 0.05). Mean arterial pressure fell from 94 +/- 2 to 47 +/- 4 mmH g just before syncope, and all subjects demonstrated sudden bradycardi a at the time of syncope. At the onset of syncope, there was sudden va sodilation and FVR fell to 26 +/- 6 units (P < 0.05 vs. baseline). Whe n the experimental forearm was treated with bretylium, phentolamine, a nd propranolol, baseline FVR fell to 26 +/- 2 units, the vasoconstrict ion during LBNP was absent, and FVR fell further to 16 +/- 1 units at syncope (P < 0.05 vs. baseline). During the second trial of LBNP, mean arterial pressure again fell to 47 +/- 4 mmHg and bradycardia was aga in observed. Treatment of the experimental forearm with the NO synthas e inhibitor N-G-monomethyl-L-arginine in addition to bretylium, phento lamine, and propranolol significantly increased baseline FVR to 65 +/- 5 units but did not prevent the marked forearm vasodilation during sy ncope (FVR = 24 +/- 4 vs. 29 +/- 8 units in the control forearm). Thes e data suggest that the profound vasodilation observed in the human fo rearm during syncope is not mediated solely by sympathetic withdrawal and also suggest that neither beta(2)-adrenergic-receptor-mediated vas e dilation nor NO is essential to observe this response.