title: Does peripheral nerve degeneration affect circulatory responses to head-up tilt in spinal cord-injured individuals?
abstract: Despite the loss of centrally mediated sympathetic vasoconstriction, spinal cord-injured (SCI) individuals cope surprisingly well with orthostatic challenges. In the pathophysiology of this intriguing observation spinal sympathetic-, veno-arteriolar-(VAR), and myogenic reflexes seem to play a role. The purpose of this study was to assess whether central (stroke volume, heart rate, blood pressure and total peripheral resistance) and peripheral (leg blood flow, leg vascular resistance and femoral arterial diameter) hemodynamic responses to head-up tilt are different in two groups of SCI patients, i. e., SCI individuals with upper motor neuron lesions (who have spinal reflexes, VAR and myogenic reflexes) (U; n=6) and those with lower motor neuron lesion (who have no spinal reflexes, perhaps no VAR due to nerve degeneration, but intact myogenic reflexes) (L; n=5). Ten healthy male individuals served as controls (C) (normal supraspinal sympathetic control and presence of all reflexes). After 10 min supine rest all individuals were tilted to 30 degrees head-up tilt. Red blood cell velocity (measured by echo Doppler ultrasound) in the femoral artery decreased and vascular resistance increased significantly in all three groups in the upright position compared with supine. Mean arterial pressure (MAP) remained unchanged in U and L and increased significantly in C in the upright versus supine position. The present study shows that all SCI individuals were able to maintain MAP by increasing leg vascular resistance during head-up tilt, despite nerve degeneration in L and lack of centrally mediated sympathetic control in all SCI individuals. Results of the present study suggest that not spinal reflexes but local (myogenic) reflex activity plays a pivotal role in peripheral vascular responses upon head-up tilt when central control mechanisms fail.
authors.affiliation: Dept. of Physiology, UMCN, 9101, 6500 HB, Nijmegen, The Netherlands.
authors.forename: Jan T
authors.initials: JT
authors.lastname: Groothuis
authors.forename: Cécile R L
authors.initials: CR
authors.lastname: Boot
authors.forename: Sibrand
authors.initials: S
authors.lastname: Houtman
authors.forename: Herman
authors.initials: H
authors.lastname: van Langen
authors.forename: Maria T E
authors.initials: MT
authors.lastname: Hopman
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D005263:Femoral Artery / Q000000981:diagnostic imaging / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D007866:Leg / Q000098:blood supply; D008297:Male; D009046:Motor Neurons / Q000502:physiology; D009410:Nerve Degeneration / Q000503:physiopathology*; D010525:Peripheral Nerves / Q000503:physiopathology*; D011187:Posture; D012039:Regional Blood Flow / Q000502:physiology; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D016683:Supine Position; D014463:Ultrasonography; D014655:Vascular Resistance / Q000502:physiology