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Neurorehabil Neural Repair · Nov 2009
Effect of treadmill training on autonomic dysreflexia in spinal cord--injured rats.
- Angela S Laird, Pascal Carrive, and Phil M E Waite.
- Department of Anatomy, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia. angela.laird@med.kuleuven.be
- Neurorehabil Neural Repair. 2009 Nov 1;23(9):910-20.
BackgroundWeight-supported treadmill training is an emerging rehabilitation method used to improve locomotor ability in patients with spinal cord injury (SCI). However, little research has been undertaken to test the effect of such training on other consequences of SCI, such as neuropathic pain and autonomic dysfunction.ObjectiveThis study investigates the effects of chronic treadmill training on the development of autonomic dysreflexia (AD), a form of cardiovascular dysfunction common in patients with cervical or high thoracic injury.MethodsTreadmill training commenced in adult male rats (n = 11) 3 days following complete T4 transection, whereas a sedentary SCI group (n = 9) and an intact group (n = 6) had no intervention. Treadmill training (up to 0.4 m/s) lasted for 10 min/d 5 days a week, for 6 weeks. Weekly measurements of locomotor ability (BBB scale), baseline mean arterial pressure, and heart rate were made, as were cardiovascular responses to training and colorectal distension (to trigger AD).ResultsTreadmill training improved BBB scores from 2 weeks post-transection onward (P = .010). However, it increased AD, resulting in augmented pressor responses from 2 to 6 weeks post-transection (P = .029). Comparison of the vascular response to phenylephrine under ganglionic blockade showed an enhanced vasoconstrictor response in the renal vasculature of trained SCI animals. Immunohistochemical comparison of the L1-L6 spinal cord segments showed an increased area of CGRP immunoreactivity in the dorsal horn (lamina III/IV) of treadmill-trained SCI compared with intact and sedentary SCI animals.ConclusionsThese results suggest that treadmill training exaggerated AD responses perhaps through a combination of enhanced vascular reactivity and central plasticity.
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