The effect of melatonin on bacterial translocation following ischemia/reperfusion injury in a rat model of superior mesenteric artery occlusion

Background: Acute mesenteric ischemia is a life-threatening vascular emergency resulting in tissue destruction due to ischemia-reperfusion injury. Melatonin, the primary hormone of the pineal gland, is a powerful scavenger of reactive oxygen species (ROS), including the hydroxyl and peroxyl radicals, as well as singlet oxygen, and nitric oxide. In this study, we aimed to investigate whether melatonin prevents harmful effects of superior mesenteric ischemia-reperfusion on intestinal tissues in rats. Methods: Rats were randomly divided into three groups, each having 10 animals. In group I, the superior mesenteric artery (SMA) was isolated but not occluded. In group II and group III, the SMA was occluded immediately distal to the aorta for 60 minutes. After that, the clamp was removed and the reperfusion period began. In group III, 30 minutes before the start of reperfusion, 10 mg/kg melatonin was administered intraperitonally. All animals were sacrified 24 hours after reperfusion. Tissue samples were collected to evaluate the I/R-induced intestinal injury and bacterial translocation (BT). Results: There was a statistically significant increase in myeloperoxidase activity, malondialdehyde levels and in the incidence of bacterial translocation in group II, along with a decrease in glutathione levels. These investigated parameters were found to be normalized in melatonin treated animals (group III). Conclusion: We conclude that melatonin prevents bacterial translocation while precluding the harmful effects of ischemia/reperfusion injury on intestinal tissues in a rat model of superior mesenteric artery occlusion. © 2015 Ozban et al.; licensee BioMed Central

in a rat model of superior mesenteric artery occlusion

We investigated whether Tempol, a water-soluble antioxidant, prevents the harmful effects of superior mesenteric ischemia/reperfusion on intestinal tissues in rats.The rats were divided into three groups of 10. In group 1, the superior mesenteric artery (SMA) was isolated but not occluded, and in groups 2 and 3 the superior mesenteric artery was occluded for 60 min. After that, the clamp was removed and reperfusion began. In group 3, 5 min before the start of reperfusion, a bolus dose of 30 mg/kg Tempol was administered intravenously and continued at a dose of 30 mg/kg for 60 min. All animals were euthanized after 24 h and tissue samples were collected for analysis.There was a significant increase in myeloperoxidase activity, malondialdehyde levels, and the incidence of bacterial translocation in group 2, with a decrease in glutathione levels. These parameters were found to be normalized in group 3. The intestinal mucosal injury score in group 2 was significantly higher than those in groups 1 and 3.Tempol prevents bacterial translocation while precluding the harmful effects of ischemia/reperfusion injury on intestinal tissues in a rat model of superior mesenteric artery occlusion