Moderate Hypothermia Protects Against Systemic Oxidative Stress in a Rat Model of Intestinal Ischemia and Reperfusion Injury

Abstract

Multisystem organ failure represents a major cause of mortality in intestinal ischemia and reperfusion (I/R), and oxidative stress plays a key role in its pathogenesis. Hypothermia is beneficial in I/R injury, but its effects on systemic oxidative stress have not been elucidated. The aim of this study was to evaluate the effects of moderate hypothermia on systemic oxidative stress after intestinal I/R injury. Anaesthetized adult rats (n = 10 per group) underwent 60 min of intestinal ischemia followed by 120 min of reperfusion or sham operation at normothermia (36 degrees C-38 degrees C) or moderate hypothermia (30 degrees C-32 degrees C). At sacrifice, ileum, liver, lungs, and kidneys were removed to determine the concentration of malondialdehyde (a marker of lipid peroxidation), reduced and oxidized glutathione (a major endogenous antioxidant), and glutathione redox state. Plasma malondialdehyde and nitrate plus nitrite (reflecting nitric oxide production) were also analyzed. A marked elevation of malondialdehyde was observed after I/R at normothermia in plasma, ileum, and lungs; however, hypothermia during I/R prevented this increase. I/R at normothermia caused a profound decrease in reduced glutathione and glutathione redox state in the ileum, but this was not observed in I/R at hypothermia. Interestingly, hypothermia increased glutathione content of control intestine. Nitric oxide production was increased only in normothermic I/R animals. Moderate hypothermia attenuates systemic oxidative stress associated with experimental intestinal I/R in an animal model by decreasing lipid peroxidation in plasma, ileum, lungs, and kidneys, by preventing the depletion of gut glutathione, and by reducing systemic nitric oxide production. However, whether these effects persist after rewarming is unknown.

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

“…5,31 In our study, intestinal I/R injury was associated with a significant decrease of SOD activity, a major endogenous antioxidant enzyme, and increase of the lipid peroxidation product MDA in the injury group. Treatment with propofol increased SOD activity and attenuated MDA production that was associated with a reduced Chiu's score (Table).…”

Protective Effects of Ascorbic Acid Pretreatment in a Rat Model of Intestinal Ischemia-Reperfusion Injury: A Histomorphometric Study

“…Support for this theory is provided by the observation that ischemic injury to the small bowel is most severe at the tip and is attenuated by intraluminal perfusion with oxygenated saline 26 . A variety of associations between ascorbic acid and IR injury has been described recently [27][28][29][30][31] . Cizova et al 27 demonstrated that the ascorbic and uric acid concentrations increased generally after IR in comparison to intact controls, but this increase was not sufficient to prevent lipid peroxidation in serum and intestinal mucosa.…”

Oxidation of Intravenous Lipid in Infants and Children With Systemic Inflammatory Response Syndrome and Sepsis

“…Plasma malondialdehyde (MDA), a measure of lipid peroxidation, was measured by high-performance liquid chromatography (33). Plasma TGs were measured spectrophotometrically (Sigma Chemical Co.) and nonesterified fatty acids (NEFAs) were measured by a spectrophotometric kit (Wako Chemical Company).…”