Abstract
The mechanisms underlying bowel dysfunction after high-level spinal cord injury (SCI)
are poorly understood. However, impaired supraspinal sympathetic and parasympathetic
control is likely a major contributing factor. Disruption of the descending autonomic
pathways traversing the spinal cord was achieved by a T3 complete spinal cord transection,
and colonic function was examined in vivo and ex vivo four weeks post-injury. Total
gastrointestinal transit time (TGTT) was reduced and contractility of the proximal
and distal colon was impaired due to reduced M3 receptor sensitivity. These data describe a clinically relevant model of bowel dysfunction
after SCI.
Keywords
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Article info
Publication history
Published online: September 01, 2018
Accepted:
August 31,
2018
Received in revised form:
August 29,
2018
Received:
November 25,
2017
Footnotes
☆Sources of funding: Killam Laureates (AAP, JWS); Heart and Stroke Foundation of Canada (AAP, AVK); MSFHR (AAP). Craig H. Neilson Foundation (AVK, AAP), Canadian Institute of Health Research, Canadian Foundation for Innovation, Paralyzed Veterans of America (AVK).
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© 2018 Elsevier B.V. All rights reserved.