Evaluation of the effects of hyperbaric oxygen treatment and enoxaparin on left colon anastomosis. An experimental study.

BACKGROUND: Surgical interventions on left colon lead to high morbidity. The problems in wound healing are the main cause of this morbidity. Hypoxia retards wound healing and hyperbaric oxygen treatment (HBOT) has an anti-hypoxic effect. MATERIALS AND METHODS: In this experimental study we divided eighty Wistar albino rats into eight groups and numbered between 1 and 8. Normal (non-ischemic) and ischemic left colon anastomosis were performed in the first and second four groups respectively. HBOT and subcutaneous enoxaparin were applied to the groups separately and in combination for four days, except the control groups. (Group-1 and Group-5). We measured anastomotic bursting pressures and performed pathological examinations besides electron microscopic study in one sample from each group after sacrificing the rats on the fourth day. RESULTS: There were no statistically significant differences in bursting pressures when we compared Group-1 with other non-ischemic groups, and Group-5 with Group-6, but there were statistically significant differences when we compared Group-5 with Group-7 and 8. In pathological examination, there were no statistically significant differences between the groups concerning necrosis, epithelization, granulation tissue formation and collagen deposition. Statistically significant differences were found in the scores of neovascularization when we compared Group-1 with Group-3 and 4, and Group-5 with Group-8. Electron microscopic evaluation revealed a prominent increase both in neovascularization and collagen fibers in the samples taken from the groups received enoxaparine and hyperbaric oxygen treatment in combination. CONCLUSIONS: These findings suggest that HBOT increases neovascularization and bursting pressures in ischemic colon anastomosis in contrast with enoxaparin.

Curcumin nutrition for the prevention of mesenteric ischemia-reperfusion injury: an experimental rodent model.

BACKGROUND: Curcumin is an anti-oxidant molecule known to be a potent inhibitor of nuclear factor-kappaB (NF-kappaB). It has been shown to attenuate ischemia/reperfusion (I/R) injury in several organ systems. In this study, we sought to investigate the effects of curcumin on the prevention of superior mesenteric artery I/R injury in rats. METHODS: Wistar albino rats were randomly allocated to 3 groups: group I, sham operated (n = 10); group II, I/R injury only (n = 10); group III, curcumin-treated I/R cohort (n = 10). Group I animals underwent laparotomy without I/R injury. After group II animals underwent laparotomy, 60 minutes of superior mesenteric artery ligation were followed by 3 hours of reperfusion. In the curcumin group, 15 days before I/R, curcumin (40 mg/kg) was administered by gastric gavage. All animals were sacrificed at the end of reperfusion. Intestinal tissue samples were obtained to investigate intestinal mucosal injury; in addition we estimated levels of myeloperoxidase (MPO) activity, malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH), interleukin (IL)-6, and tumor necrosis factor (TNF)-alpha. RESULTS: There were statistically significant decreases in GSH levels, along with an increase in intestinal mucosal injury scores, MPO activity, MDA levels, NO, IL-6, and TNF-alpha in group I when compared with groups II and III (P = .01). Curcumin treatment in group III produced a significant increase in GSH levels, as well as a decrease in intestinal mucosal injury scores, MPO activity, MDA, and NO levels when compared with group II (P < .05). CONCLUSION: This study showed that curcumin treatment significantly attenuated reperfusion injury in a superior mesenteric artery I/R model in rats.