Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans.

Our aim was to determine whether sympathetic withdrawal alone can account for the profound forearm vasodilation that occurs during syncope in humans. We also determined whether either vasodilating beta 2-adrenergic receptor or nitric oxide (NO) contributes to this dilation. Forearm blood flow was measured bilaterally in healthy volunteers (n = 10) by using plethysmography during two bouts of graded lower body negative pressure (LBNP) to syncope. In one forearm, drugs were infused via a brachial artery catheter while the other forearm served as a control. In the control arm, forearm vascular resistance (FVR) increased from 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 mmHg just before syncope, and all subjects demonstrated sudden bradycardia at the time of syncope. At the onset of syncope, there was sudden vasodilation and FVR fell to 26 +/- 6 units (P < 0.05 vs. baseline). When the experimental forearm was treated with bretylium, phentolamine, and propranolol, baseline FVR fell to 26 +/- 2 units, the vasoconstriction 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 again observed. Treatment of the experimental forearm with the NO synthase inhibitor NG-monomethyl-L-arginine in addition to bretylium, phentolamine, and propranolol significantly increased baseline FVR to 65 +/- 5 units but did not prevent the marked forearm vasodilation during syncope (FVR = 24 +/- 4 vs. 29 +/- 8 units in the control forearm). These data suggest that the profound vasodilation observed in the human forearm during syncope is not mediated solely by sympathetic withdrawal and also suggest that neither beta 2-adrenergic-receptor-mediated vasodilation nor NO is essential to observe this response.