Gastric dysreflexia after acute experimental spinal cord injury in rats

Gastric reflexes are mediated mainly by vago‐vagal reflex circuits in the caudal medulla. Despite the fact that brainstem vago‐vagal circuitry remains intact after spinal cord injury (SCI), patients with SCI at the cervical level most often present gastric stasis with an increased risk of reflux and...

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Bibliographic Details
Published in:Neurogastroenterology and motility 2009-02, Vol.21 (2), p.197-206
Main Authors: Tong, M., Holmes, G. M.
Format: Article
Language:English
Subjects:
Animals
Autonomic Dysreflexia - etiology
Autonomic Dysreflexia - physiopathology
Eating
Ganglia, Sympathetic - pathology
gastric motility
Gastrointestinal Motility - physiology
Gastroparesis - physiopathology
Humans
Male
Motor Activity - physiology
neurotrauma
Random Allocation
Rats
Rats, Wistar
receptive relaxation reflex
Reflex - physiology
Spinal Cord Injuries - complications
Spinal Cord Injuries - pathology
Spinal Cord Injuries - physiopathology
Stomach - physiopathology
vagovagal reflex
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Summary:Gastric reflexes are mediated mainly by vago‐vagal reflex circuits in the caudal medulla. Despite the fact that brainstem vago‐vagal circuitry remains intact after spinal cord injury (SCI), patients with SCI at the cervical level most often present gastric stasis with an increased risk of reflux and aspiration of gastric contents. Using a miniature strain gauge sutured to the gastric surface; we tested gastric motility and reflexive gastric relaxation following oesophageal distension (oesophageal‐gastric relaxation reflex) in animals 3 days after a severe spinal contusion at either the third or ninth thoracic spinal segment (acute T3‐ or T9 SCI, respectively). Both basal gastric motility and the oesophageal‐gastric relaxation reflex were significantly diminished in animals with T3 SCI. Conversely, both basal gastric motility and the oesophageal‐gastric relaxation reflex were not significantly reduced in T9 SCI animals compared to controls. The reduced gastric motility and oesophageal‐gastric reflex in T3 SCI rats was not ameliorated by celiac sympathectomy. Our results show that gastric stasis following acute SCI is independent of altered spinal sympathetic input to the stomach caudal to the lesion. Our data suggest that SCI may alter the sensitivity of vagal reflex function, perhaps by interrupting ascending spinosolitary input to brainstem vagal nuclei.
ISSN:1350-1925
1365-2982
DOI:10.1111/j.1365-2982.2008.01215.x