Autonomic dysreflexia is a hypertensive episode in spinal cord–injured individuals induced by exaggerated sympathetic activity and thought to be -adrenergic mediated.

-Adrenoceptor antagonists have been a rational first choice; nevertheless, calcium channel blockers are primarily used in autonomic dysreflexia management.

However, -adrenoceptor blockade may leave a residual vasoconstrictor response to sympathetic nonadrenergic transmission unaffected.

The aim was to assess the -adrenergic contribution and, in addition, the role of supraspinal control to leg vasoconstriction during exaggerated sympathetic activity provoked by autonomic dysreflexia in spinal cord–injured individuals and by a cold pressure test in control individuals.

Upper leg blood flow was measured using venous occlusion plethysmography during supine rest and during exaggerated sympathetic activity in 6 spinal cord–injured individuals and 7 able-bodied control individuals, without and with phentolamine (-adrenoceptor antagonist) and nicardipine (calcium channel blocker) infusion into the right femoral artery.

Leg vascular resistance was calculated. In spinal cord–injured individuals, phentolamine significantly reduced the leg vascular resistance increase during autonomic dysreflexia (8±5 versus 24±13 arbitrary units; P=0.04) in contrast to nicardipine (15±10 versus 24±13 arbitrary units; P=0.12).

In controls, phentolamine completely abolished the leg vascular resistance increase during a cold pressure test (1±2 versus 18±14 arbitrary units; P=0.02).

The norepinephrine increase during phentolamine infusion was larger (P=0.04) in control than in spinal cord–injured individuals.

These results indicate that the leg vascular resistance increase during autonomic dysreflexia in spinal cord–injured individuals is not entirely -adrenergic mediated and is partly explained by nonadrenergic transmission, which may, in healthy subjects, be suppressed by supraspinal control.

Key Words: autonomic dysreflexia • spinal cord injury • sympathetic nervous system • neurotransmitters • leg vascular resistance

Jan T. Groothuis; Gerard A. Rongen; Jaap Deinum; Peter Pickkers; A. H. Jan Danser; Alexander C.H. Geurts; Paul Smits; Maria T.E. Hopman

From the Departments of Physiology (J.T.G., M.T.E.H.), Pharmacology-Toxicology (G.A.R., P.S.), General Internal Medicine (J.D.), Intensive Care Medicine (P.P.), and Rehabilitation (A.C.H.G.), Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; Department of Rehabilitation (J.T.G., A.C.H.G.), Sint Maartenskliniek, Nijmegen, The Netherlands; Division of Pharmacology, Vascular and Metabolic Diseases (A.H.J.D.), Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands.

Correspondence to Maria T.E. Hopman, Department of Physiology, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands. E-mail m.hopman@fysiol.umcn.nl