Neural and anatomical abnormalities of the gastrointestinal system resulting from contusion spinal cord injury

Abstract

Gastrointestinal (GI) abnormalities resulting from spinal cord injury (SCI) are challenging disorders that have not been examined experimentally using clinically relevant models. In this study, female Sprague–Dawley rats (n=5/group×4: T10–T11 contusion, laminectomy, or naïve) were fasted for 24 h before being submitted to dye recovery assays (Phenol Red solution, 1.5 ml/rat; per oral) on GI emptying/transiting at 48 h or 4 weeks postinjury (p.i.). Compared with controls, SCI significantly increased dye recovery rate (DRR, determined by spectrophotometry) in the duodenum (+84.6%) and stomach (+32.6%), but decreased it in the jejunum (−64.1% and −49.5%) and ileum (−73.6% and −70.1%) at 48 h and 4 weeks p.i., respectively (P≤0.005, ANOVA with post hoc t-test). Electrophysiological analysis revealed that purinergic fast inhibitory junction potential (IJP) was reduced ∼30% in the antrum and duodenum of rats 48 h p.i. (numbers of animals/numbers of tissue samples=3/7; P<0.001), and slow IJP was essentially abolished. Immunocytochemistry consequently uncovered significant reductions in the GI vasoactive intestinal polypeptide and neuronal nitric oxide synthase (i.e. slow IJP mediators) reactivity at 48 h and 4 weeks p.i., suggesting that SCI disrupted interstitial neurotransmission. Importantly, SCI caused discernible atrophy of the GI mucosa and muscle coat (e.g. the two layers of gastric wall were correspondingly 28% and 27% thinner 4 weeks p.i.). We conclude that contusive SCI triggers GI abnormalities with unique pathophysiology and pathology in different segments. Such GI disorders evolve continuously during the entire post-SCI period examined, and may require therapeutic development to target specific underlying mechanisms.