Reduced colonic smooth muscle cholinergic responsiveness is associated with impaired bowel motility after chronic experimental high-level spinal cord injury.

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 M receptor sensitivity. These data describe a clinically relevant model of bowel dysfunction after SCI.