Increased intestinal permeability in rats subjected to traumatic frontal lobe percussion brain injury

Background: Dysfunction of the gastrointestinal-(Gl} tracns-a common-occurrence following traumatic brain injury (TBI). We hypothesised that increased intestinal permeability may result from a precisely controlled percussion injury to the exposed brains of anaesthetised rats and that such an effect could be assessed in vitro using excised intestinal mucosae mounted in Ussing chambers. Methods: Following craniotomy over the left medial prefrontal cortex on anaesthetised rats, neurotrauma was produced using a pneumatically-driven impactor on the exposed brain. Control rats were subjected to identical procedures but did not receive an impact. Muscle-stripped rat intestinal ileal and colonic segments were mounted in Ussing chambers within 30 minutes of death. Transepithelial electrical resistance (TEER) and the apparent permeability coefficient (Papp) of[14C)-mannitol were recorded from intestinal tissue for 120 minutes. Histopathology was also carried out to determine any gross morphological changes in the intestine. Results: Ileal and colonic mucosae showed no differences in TEER in ileum or colon ofTBI rats compared to controls. The Papp of mannitol was significantly increased in ilea from rats previously exposed to TBI compared to controls. Histological analysis showed gross changes to 50% of the ileal but not the colonic sections from TBI rats. Conclusion: TBI results in significantly reduced ileal barrier function, most likely mediated by open tight junctions. For patients with acute head injury, this may have implications for subsequent oral absorption of nutrients. Systemic delivery of luminal endotoxins may contribute to multiple organ failure.