International Collaboration on Repair Discoveries, University of British Columbia, Canada.
International Collaboration on Repair Discoveries, University of British Columbia, Canada; Experimental Medicine Program, University of British Columbia, Canada; Department of Physiology and Pharmacology, Hotchkiss Brain Institute, Libin Cardiovascular Institute, Cumming School of Medicine, University of Calgary, Canada.
Auton Neurosci. 2019 Jan;216:33-38. doi: 10.1016/j.autneu.2018.08.005. Epub 2018 Sep 1.
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.
高水平脊髓损伤（SCI）后肠道功能障碍的机制尚不清楚。然而，脊髓上交感神经和副交感神经控制受损可能是主要的促成因素。通过 T3 完全性脊髓横断破坏了穿过脊髓的下行自主神经通路，并在损伤后 4 周进行了体内和体外的结肠功能检查。由于 M 受体敏感性降低，总胃肠传输时间（TGTT）缩短，近端和远端结肠的收缩性受损。这些数据描述了 SCI 后肠道功能障碍的一种具有临床相关性的模型。
