Abstract
BackgroundThe aim of the present study was to test the potential protective effects of the organic vanadium salt bis (maltolato) oxovanadium (BMOV; 15 mg/kg) in the context of renal ischemia/reperfusion (30 min of ischemia) and its effects on renal oxygenation and renal function in the acute phase of reperfusion (up to 90 min post-ischemia).MethodsIschemia was established in anesthetized and mechanically ventilated male Wistar rats by renal artery clamping. Renal microvascular and venous oxygenation were measured using phosphorimetry. Creatinine clearance rate, sodium reabsorption, and renal oxygen handling efficiency were considered markers for renal function.ResultsThe main findings were that BMOV did not affect the systemic and renal hemodynamic and oxygenation variables and partially protected renal sodium reabsorption.ConclusionsPretreatment with the organic vanadium compound BMOV did not protect the kidney from I/R injury.
Highlights
The aim of the present study was to test the potential protective effects of the organic vanadium salt bis oxovanadium (BMOV; 15 mg/kg) in the context of renal ischemia/reperfusion (30 min of ischemia) and its effects on renal oxygenation and renal function in the acute phase of reperfusion
Increased production of radical oxygen species (ROS) and reactive nitrogen species (RNS) [10,11,12,13] and a regional imbalance between vasoactive mediators are believed to be of great importance in the development of Acute kidney injury (AKI) by leading impaired microcirculatory perfusion and to cellular damage, apoptosis, and irreversible organ failure [4,5]
There were no significant differences between groups in any of these variables
Summary
The aim of the present study was to test the potential protective effects of the organic vanadium salt bis (maltolato) oxovanadium (BMOV; 15 mg/kg) in the context of renal ischemia/reperfusion (30 min of ischemia) and its effects on renal oxygenation and renal function in the acute phase of reperfusion (up to 90 min post-ischemia). Acute kidney injury (AKI) is a frequent and costly clinical complication in critically ill patients. Using the RIFLE criteria in 20,126 hospitalized patients, Uchino et al has found that 20% of the patients had some degrees of acute renal impairment and 3.7% of these patients had AKI [1]. In addition to hypoxic hit consequent to ischemia, the reperfusion phase has been associated with additional renal injury. Increased production of radical oxygen species (ROS) and reactive nitrogen species (RNS) [10,11,12,13] and a regional imbalance between vasoactive mediators are believed to be of great importance in the development of AKI by leading impaired microcirculatory perfusion and to cellular damage, apoptosis, and irreversible organ failure [4,5]
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