Wang Huaxin, Chen Hui, Wang Lei, Liu Lin, Wang Min, Liu Xiuheng
Department of Urology, Renmin Hospital, Wuhan University, Wuhan, China.
Department of Urology, Renmin Hospital, Wuhan University, Wuhan, Hubei, China.
Acta Cir Bras. 2014 Dec;29(12):812-8. doi: 10.1590/S0102-86502014001900008.
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.
探讨急性高血糖对右美托咪定诱导的肾缺血再灌注损伤预处理作用的影响。
将Sprague-Dawley大鼠随机分为正常血糖组（NG）和高血糖组（HG），每组再分为假手术组（无缺血/再灌注损伤）、缺血/再灌注组（I/R）和右美托咪定组（给予右美托咪定）。在缺血前45分钟腹腔注射（i.p.）25%葡萄糖（3 g/kg）诱导急性高血糖。在诱导缺血前30分钟腹腔注射右美托咪定（50 μg/kg）。检测肾功能、组织学、细胞凋亡、Bax、Bcl-2和磷酸化AKT（p-AKT）的表达。
缺血/再灌注损伤显著升高血清尿素氮和肌酐水平、肾小管上皮细胞凋亡、Bax和p-AKT的表达，但降低Bcl-2的表达。高血糖进一步加重了所有这些变化（p<0.05）。在高血糖条件下，缺血/再灌注组和右美托咪定组在上述所有检测指标上均无统计学差异（p>0.05）。
急性高血糖减弱了右美托咪定诱导的非糖尿病大鼠肾缺血再灌注损伤预处理作用。
