Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans

Niki M. Dietz, John R. Halliwill, John M. Spielmann, Lori A. Lawler, Bettina G. Papouchado, Tamara J. Eickhoff, and Michael J. Joyner Departments of Anesthesiology and of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905 Received 15 August 1996; accepted in final form 5 February 1997. Dietz, Niki M., John R. Halliwill, John M. Spielmann, Lori A. Lawler, Bettina G. Papouchado, Tamara J. Eickhoff, and Michael J. Joyner. Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans. J. Appl. Physiol. 82(6): 1785-1793, 1997. 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 2 -adrenergic receptors 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