Abstract
BackgroundAcute 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.MethodsRats 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).ResultsThere 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).ConclusionWe 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.
Highlights
Acute mesenteric ischemia is a life-threatening vascular emergency resulting in tissue destruction due to ischemia-reperfusion injury
Bacterial translocation The incidence of bacterial translocation to the mesenteric lymph nodes (MLN) (P = 0.0001), liver (P = 0.008), and spleen (P = 0.036) was significantly higher in I/R only animals than in sham operated and melatonin treated animals (Table 1)
The incidence of translocation was not statistically different in melatonin treated group from the value measured in sham operated group of animals for each location (P = 0.14 for MLN, P = 0.14 for liver, P = 1.00 for spleen)
Summary
Acute mesenteric ischemia is a life-threatening vascular emergency resulting in tissue destruction due to ischemia-reperfusion injury. 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. The injured intestinal mucosa loses its resistance to indigenous enteric microorganisms, which leads to translocation of bacteria to extraintestinal sites such as mesenteric lymph nodes, liver, spleen, and blood [5]. This bacterial translocation may play an important role in the development of sepsis and multiple organ system failure [1]. We aimed to investigate whether melatonin precludes bacterial translocation after intestinal ischemia-reperfusion injury in rats
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