Abstract
To investigate the effects of acute hyperglycemia on dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury. Sprague-Dawley rats were randomly arranged to the normoglycemic (NG) or hyperglycemic group (HG), with each group further divided into sham (no I/R injury), I/R (ischemia-reperfusion) and dex (given by dexmedetomidine) groups. Acute hyperglycemia was induced by intraperitoneal injection (i.p.) of 25% glucose (3 g/kg) 45 min before ischemia. Dexmedetomidine (50 μg/kg, i.p.) was administrated 30 min before induction of ischemia. Renal function, histology, apoptosis, expression of Bax, Bcl-2 and phosphorylated AKT (p-AKT) were detected. I/R insult significantly increased the serum levels of blood urea nitrogen and creatinine, apoptotic tubular epithelial cells, expression of Bax and p-AKT, but decreased Bcl-2 expression. All these changes were further enhanced by hyperglycemia (p<0.05). In hyperglycemic condition, there was no statistically difference between the I/R group and Dex group in all the aforementioned detection indexes (p>0.05). Acute hyperglycemia attenuates dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury in non-diabetic rats.
Highlights
Groups and drug administrationIschemia-reperfusion (I/R)-induced renal injury remains a leading cause of delayed graft dysfunction and chronic allograft nephropathy after kidney transplantation[1]
Not uncommon in non-diabetic patients after renal transplantation, could accentuate renal ischemic injury, apoptosis, antigen presentation and inflammatory responses which might increase the risk of graft rejection[8]
Two anesthetics, i.e. propofol and isoflurane, lost their protective effect of renal I/R injury during transient hyperglycemia[11]. It is still unclear whether acute hyperglycemia before I/R could compromise the protective effects of dexmedetomidine-induced preconditioning
Summary
Groups and drug administrationIschemia-reperfusion (I/R)-induced renal injury remains a leading cause of delayed graft dysfunction and chronic allograft nephropathy after kidney transplantation[1]. Dexmedetomidine, a commonly used anesthetic, could exert renoprotective effects on normoglycemic animals when administered before renal I/R4-6. Previous studies have proved that hyperglycemia could render the cardiopreotective effects of anesthetic preconditioning counterproductive[9,10]. Two anesthetics, i.e. propofol and isoflurane, lost their protective effect of renal I/R injury during transient hyperglycemia[11]. It is still unclear whether acute hyperglycemia before I/R could compromise the protective effects of dexmedetomidine-induced preconditioning. The major purpose of this study was to investigate whether the impact of acute hyperglycemia were refractory to protection induced by dexmedetomidine preconditioning in a rat model
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