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Passive Leg Cycling Comprehensively Restores Cerebrovascular Health After Experimental High‐thoracic Spinal Cord Injury
Author(s) -
Jia Mengyao,
Phillips Aaron A.,
Matin Nusrat,
Yung Andrew,
Zheng Mei Mu Zi,
Lee Amanda,
Monga Aaron,
Kozlowski Piotr,
Dorrence Anne,
Krassioukov Andrei V.
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1077.13
Subject(s) - medicine , spinal cord injury , spinal cord , hindlimb , cerebral blood flow , middle cerebral artery , blood flow , anesthesia , stroke (engine) , cerebral arteries , cardiology , ischemia , psychiatry , engineering , mechanical engineering
Individuals living with chronic spinal cord injury exhibit a 3–4 fold increased risk of stroke. Reduced cerebral blood flow following is associated with cognitive decline, increased risk of stroke, and development of white matter irregularities. Previously, we have reported impairment in cerebrovascular health following experimental high‐thoracic spinal cord injury, including cerebrovascular reactivity declines, as well as inward remodelling and profibrosis of the middle cerebral artery. Passive hind‐limb exercise after spinal cord injury has been shown to restore systemic cardiovascular function, however it has never been explored for improving cerebrovascular health. Objective To preclinically investigate the effect of passive hind‐limb exercise in preventing cerebrovascular decline following high‐thoracic spinal cord injury. Design/Method Male Wistar rats (n=45) were uninjured, T3‐level complete transected or T3‐transected with passive exercise. Six days after surgery, the hind‐limb passive cycling intervention was initiated and lasted for five weeks. Six weeks after surgery, Magnetic resonance imaging was performed to evaluate baseline cerebral blood flow. Middle cerebral arteries were then harvested for functional and structural assessments, including in vitro pressure myography and immunohistochemistry. Conclusion There was a 44% reduction in global cerebral blood flow ( p =0.001) after spinal cord injury, which was restored with passive exercise ( Figure 1). Passive exercise also prevented the endothelial dysfunction seen after spinal cord injury ( p =0.046). Profibrotic remodelling of middle cerebral arteries demonstrated by increased collagen (95%, p =0.004), was also reversed by passive exercise. As such, passive hind‐limb cycling is effective in restoring healthy brain blood flow, endothelial function, and preventing profibrosis in the cerebral vasculature. Clearly, passive exercise is a promising pre‐clinical therapy to restore cardiovascular health after spinal cord injury, and the present data extend these benefits even to the brain. Support or Funding Information Support: AAP: Killam Trust, Craig H. Neilsen Foundation Postdoctoral Fellowship 337427, Heart and Stroke Foundation of Canada Research Fellowship, Michael Smith Foundation for Health Research Postdoctoral Fellowship AVK: Canadian Institute of Health Research, Craig H. Neilsen Foundation.