A ferret model of acute multifocal gastrointestinal infarction.
Based on the demonstration of mural granulomatous vasculitis in Crohn's disease, it was hypothesized that this vasculitis may account for the discontinuous pattern of lesions in this condition. Accordingly, the present study investigated the histological changes produced by interruption of the submucosal and mucosal microcirculation in the ferret midgut. Two techniques were used. First, up to 30 adjacent vasa recta were ligated using microsurgical techniques; this produced no evidence of ischemic damage. Second, interruption of the submucosal collateral plexus by the intra-arterial injection of styrene microspheres (27-, 50-, or 90-microns diameter) produced acute intestinal mucosal damage. A combination of 27- and 90-microns spheres resulted in focal mucosal inflammation, necrosis, and ulceration. "Summit" lesions with normal adjacent mucosa were observed 48 hours after embolization, with evidence of regeneration of the mucosa overlying the occluded vessels at 72 hours. This model shows that focal gastrointestinal infarction with normal adjacent mucosa can be produced by acute occlusion of submucosal and mucosal arteries.[1]References
- A ferret model of acute multifocal gastrointestinal infarction. Hudson, M., Piasecki, C., Sankey, E.A., Sim, R., Wakefield, A.J., More, L.J., Sawyerr, A.M., Dhillon, A.P., Pounder, R.E. Gastroenterology (1992) [Pubmed]
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