Nm. Dietz et al., SYMPATHETIC WITHDRAWAL AND FOREARM VASODILATION DURING VASOVAGAL SYNCOPE IN HUMANS, Journal of applied physiology, 82(6), 1997, pp. 1785-1793
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.