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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Acute Disease, Animals, Apoptosis, Blood Glucose, Creatinine, Dexmedetomidine, Hyperglycemia, Ischemia, Ischemic Preconditioning, Kidney, Kidney Tubules, Male, Models, Animal, Nephrectomy, Proto-Oncogene Proteins c-akt, Random Allocation, Rats, Sprague-Dawley, Reperfusion Injury, Urea.
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Does acute hyperglycemia prevent dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury? Context: 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).
assistant
Acute hyperglycemia attenuates dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury in non-diabetic rats. Final Decision: yes