Abstract
Introduction: Preoperative gastric ischemic conditioning (IC) improves the outcome of esophageal replacement gastroplasty and is associated with low morbidity. However, when the stomach cannot be used for esophageal replacement, a colonic replacement is required. The study aim was to assess the viability of right colon and terminal ileum IC in a rat model and the histological damage/recovery sequence and determine if neovascularization is a potential adaptive mechanism. Methods: The study was conducted in Rattus norvegicus with ileocolic vascular ligation. Seven groups of animals were established (6 rats per group) with groups defined by the date of their post-IC euthanasia (+1, +3, +6, +10, +15, and +21 days). Comparisons were made with a sham group. Viability of the model was defined as <10% of transmural necrosis. The evaluation of histological damage used the Chiu score in hematoxylin and eosin sections of paraffin-embedded specimens with CD31 immunohistochemical assessment of neovascularization by the median of submucosal vessel counts in 5 high-magnification fields. Results: Transmural colon necrosis occurred in 1/36 animals (2.78%) with no animal demonstrating transmural ileal necrosis. The maximum damage was observed in the colon on +1 day post-IC (average Chiu score 1.67, p = 0.015), whereas in the ileum, it was on days +1, +3, and +6 (average Chiu score 1.5, 1.3, and 1.17; p = 0.015, 0.002, and 0.015, respectively). In the +21-day group, histological recovery was complete in the colon in 4 (66.7%) of the 6 animals and in the ileum in 5 (83.3%) of 6 animals. There were no significant differences in quantitative neovascularization in any of the groups when compared with the sham group or when comparisons were made between groups. Conclusions: The tested animal model for IC of the colon and terminal ileum appeared to be feasible. Histological damage was maximal between the 1st and 3rd day following IC, but by day 21, recovery was complete in two-thirds of the rats. There was no evidence in this preliminary IC model that would suggest neovascularization as an adaptive mechanism.