Mechanistic involvement of noradrenergic neuronal neurotransmitter release in cutaneous vasoconstriction during autonomic dysreflexia in persons with spinal cord injury.

Introduction: Autonomic dysreflexia (AD) is a potentially life-threatening consequence in high (above T6) spinal cord injury that involves multiple incompletely understood mechanisms. While peripheral arteriolar vasoconstriction, which controls systemic vascular resistance, is documented to be pronounced during AD, the pathophysiological neurovascular junction mechanisms of this vasoconstriction are undefined. One hypothesized mechanism is increased neuronal release of norepinephrine and co-transmitters.

Elucidating mechanisms of attenuated skin vasodilation during passive heat stress in persons with spinal cord injury.

Objective: Persons with spinal cord injury (SCI) are unable to efficiently dissipate heat via thermoregulatory vasodilation as efficiently as able-bodied persons during whole body passive heat stress (PHS). Skin blood flow (SkBF) is controlled by dual sympathetic vasomotor systems: noradrenergic vasoconstrictor (VC) nerves and cholinergic vasodilator (VD) nerves. Thus, impaired vasodilation could result from inappropriate increases in noradrenergic VC tone that compete with cholinergic vasodilation or diminished cholinergic tone.

Are Thermoregulatory Sweating and Active Vasodilation in Skin Controlled by Separate Nerves During Passive Heat Stress in Persons With Spinal Cord Injury?

Background: Sudomotor responses (SR) and active vasodilation (AVD) are the primary means of heat dissipation during passive heat stress (PHS). It is unknown if they are controlled by a single or separate set of nerves. Older qualitative studies suggest that persons with spinal cord injury (SCI) have discordant areas of sweating and vasodilation.