ABSTRACT
BACKGROUND: This study aims to investigate the effect of ozone on myocardial ischemia-reperfusion injury occurring after occlusion - reperfusion of infrarenal abdominal aorta in rats. METHODS: Thirty-two Wistar albino rats (weighing 200-250 g) were randomized into four equal groups. The control (sham) group underwent laparotomy and dissection of the infrarenal abdominal aorta without occlusion. Intraperitoneal ozone was applied for 10 days 1 mg/kg/day in the control+ozone group. Afterwards, control+ozone group underwent laparotomy and dissection of the infrarenal abdominal aorta without occlusion. Aortic ischemia-reperfusion and aortic ischemia-reperfusion+ozone groups underwent dissection of the infrarenal abdominal aorta, followed by achieving ischemia and reperfusion by cross-clamping the infrarenal abdominal aorta for 60 minutes and removing the cross-clamp for 60 minutes, respectively. The tissue levels of malondialdehyde and activity levels of superoxide dismutase, catalase, and myeloperoxidase were measured in the myocardial specimens. The tumor necrosis factor, interleukin-6 and troponin-I levels were measured in the plasma. A histopathological examination of the myocardial specimens was undertaken. RESULTS: Biochemical analysis showed that aortic ischemia-reperfusion significantly increased (p<0.05 vs. control) while ozone significantly decreased (p<0.05 vs. aortic ischemia-reperfusion) the myocardial tissue levels of superoxide dismutase and catalase and level of plasma troponin-I. Histologically, in the aortic ischemia-reperfusion group, myocardial disorganization, myofiber swelling and myofiber eosinophilia in the myocardial tissue samples were significantly increased compared to the control group (p<0.05 vs. control). However, histopathological changes in the aortic ischemia-reperfusion+ozone group decreased compared to the aortic ischemia-reperfusion group. CONCLUSION: The results of this experimental study indicate that ozone attenuates myocardial injury and oxidative stress that develop after infrarenal aortic ischemia-reperfusion through three markers; (i) decreased tissue superoxide dismutase and catalase levels, (ii) d ecreased p lasma t roponin-I l evels, a nd (iii) reduced histopathological changes, albeit not statistically significant.
ABSTRACT
BACKGROUND: Aortic ischemia-reperfusion (IR) is an important factor in the development of postoperative acute lung injury following abdominal aortic surgery. The aim of our study was to examine the effect of ß-glucan on lung injury induced by abdominal aortic IR in rats. MATERIAL AND METHODS: Thirty-two Wistar-albino rats were randomized into four groups (eight per group) as follows: the control group (sham laparotomy), aortic IR (120 min ischemia and 120 min reperfusion), aortic IR + ß-glucan (ß-glucan 50 mg/kg/d for 10 d was administered orally before IR), and control + ß-glucan. Lung tissue samples were obtained for biochemical analysis. Protein concentrations in bronchoalveolar lavage fluid and lung wet/dry weight ratios were measured. Histologic evaluation of the rat lung tissues was also performed. RESULTS: Aortic IR significantly increased the levels of MDA, superoxide dismutase, catalase, and myeloperoxidase (P < 0.05 versus control).Whereas, ß-glucan significantly decreased the lung tissue levels of MDA, superoxide dismutase, catalase, myeloperoxidase, (P < 0.05 versus aortic IR), and protein concentration in bronchoalveolar lavage fluid as well as wet/dry lung weight ratio. Histologic evaluation showed that ß-glucan attenuated the morphological changes associated with lung injury. CONCLUSIONS: The results of this study indicate that ß-glucan attenuates lung injury induced by aortic IR in rats. We propose that this protective effect of ß-glucan is due to (1) reduced systemic inflammatory response, (2) reduced oxidative stress and lipid peroxidation in the lung tissue, (3) reduced pulmonary microvascular leakage, and (4) inhibition of leukocyte infiltration into the lung tissue.
