Abstract
Renal ischemia/reperfusion injury is a common cause of acute kidney injury (AKI) and hypertension might contribute to the increased incidence of AKI. The purpose of this study was to investigate the effects of single and combined hyperbaric oxygen (HBO) preconditioning and NADPH oxidase inhibition on oxidative stress, kidney function and structure in spontaneously hypertensive rats (SHR) after renal ischemia reperfusion injury. HBO preconditioning was performed by exposing to pure oxygen (2.026 bar) twice a day for two consecutive days for 60 minutes, and 24h before AKI induction. For AKI induction, the right kidney was removed and ischemia was performed by clamping the left renal artery for 45 minutes. NADPH oxidase inhibition was induced by apocynin (40 mg/kg b.m., intravenously) 5 minutes before reperfusion. AKI significantly increased renal vascular resistance and reduced renal blood flow, which were significantly improved after apocynin treatment. Also, HBO preconditioning, with or without apocynin treatment showed improvement on renal hemodynamics. AKI significantly increased plasma creatinine, urea, phosphate levels and lipid peroxidation in plasma. Remarkable improvement, with decrease in creatinine, urea and phosphate levels was observed in all treated groups. HBO preconditioning, solitary or with apocynin treatment decreased lipid peroxidation in plasma caused by AKI induction. Also, combined with apocynin, it increased catalase activity and solitary, glutathione reductase enzyme activity in erythrocytes. While AKI induction significantly increased plasma KIM– 1 levels, HBO preconditioning, solitary or with apocynin decreased its levels. Considering renal morphology, significant morphological alterations present after AKI induction were significantly improved in all treated groups with reduced tubular dilatation, tubular necrosis in the cortico-medullary zone and PAS positive cast formation. Our results reveal that NADPH oxidase inhibition and hyperbaric oxygen preconditioning, with or without NADPH oxidase inhibition may have beneficial effects, but their protective role should be evaluated in further studies.
Highlights
Acute kidney injury (AKI) is associated with significant in-hospital morbidity and mortality, in those admitted to the Intensive care units, where mortality rates may exceed 50% [1]
The animals were randomly divided into five experimental groups: sham-operated rats (SHAM, n = 9), rats with induced postischemic AKI (AKI, n = 11), animals with AKI and apocynin treatment (AKI+APO, n = 11), group with hyperbaric oxygen (HBO) preconditioning before AKI inducing (AKI+HBO, n = 14) and group with HBO preconditioning before and apocynin treatment after AKI induction (AKI+APO+HBO, n = 13)
In AKI group heart rate (HR) was significantly decreased in comparison to SHAM (p
Summary
Acute kidney injury (AKI) is associated with significant in-hospital morbidity and mortality, in those admitted to the Intensive care units, where mortality rates may exceed 50% [1]. There are chronic consequences that carry high risk of developing or exacerbating chronic kidney disease and accelerated development of the endstage renal disease [2] Several factors, such as hypertension [3], invasive diagnostic procedures and complex surgery, especially cardiothoracic surgery, partial nephrectomy, renal transplantation or renal stone surgery might contribute to the increased incidence of AKI [4]. Oxidative stress has a very important role in renal damage, and opens potential targets for therapeutic intervention It both directly and indirectly affects all aspects of the kidney, including vascular reactivity, renal hemodynamics, glomerular filtration, tubular reabsorption and secretion in all nephron segments [8]
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