NEUROSCIENCE, vol.154, no.4, pp.1627-1638, 2008 (SCI-Expanded)
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 x 4: T10-T11 contusion, laminectomy, or naive) were fasted for 24 In 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 In 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 similar to 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. Published by Elsevier Ltd on behalf of IBRO.