ABSTRACT
Objective To evaluate the effect of remifentanil on cell apoptosis during renal ischemia-reperfusion (I/R) in rats.Methods Seventy-five male Sprague-Dawley rats,weighing 220-250 g,were randomly divided into 3 groups (n =25 each):sham operation group (group S),I/R group,and remifentanil group (group R).Renal ischemia was induced by occlusion of the bilateral renal arteries for 45 min followed by reperfusion in groups I/R and R.Remifentanil was infused at 1.0 μg· kg-1 · min-1 via the caudal vein starting from 15 min before ischemia until 30 min of reperfusion in group R,while the equal volume of normal saline was given instead of remifentanil in groups S and I/R.At 15 min before ischemia (T0) and 3,6,12,24 h of reperfusion (T1-4),5rats were anesthetized and sacrificed,and renal specimens were obtained to detect the apoptotic rate and expression of Bax and Bcl-2 protein (by flow cytometry) and mRNA (by RT-PCR).The ratios between Bcl-2/Bax protein and mRNA expression were calculated.The pathological changes of renal tubules were scored.Results Compared with group S,the pathological scores and apoptotic rate were significantly increased at T1-4,and ratios between Bcl-2/Bax protein and mRNA expression were increased at T1,2,while decreased at T3,4 in groups R and I/R (P ＜0.01).Compared with group I/R,the pathological scores and apoptotic rate were significantly decreased at T1-4,while the ratios between Bcl-2/Bax protein and mRNA expression were increased in group R (P ＜ 0.05 or 0.01).Compared with the baseline value at T0,the pathological scores and apoptotic rates were significantly increased at T1 4,and the ratios of Bcl-2/Bax protein and mRNA expression were increased at T1,2,while decreased at T3,4 in groups R and I/R (P ＜ 0.01).Conclusion Regulation of Bcl-2/Bax expression and inhibition of cell apoptosis in renal tissues are involved in the mechanism by which remifentanil reduces renal I/R injury in rats.
ABSTRACT
Objective To investigate the effects of different doses of remifentanil on the renal ischemiareperfusion (I/R) injury in rats. Methods Sixty male SD rats weighing 220-250 g were randomly divided into 5 groups ( n = 12 each): sham operation group (group S), model group (group M), low, median and high doses of remifentanil groups (RL, RM and RH groups). The rats were anesthetized with intraperitoneal 5% chloral hydrate 6 ml/kg. Renal ischemia was induced by clamping the bilateral renal arteries for 45 min using an atraumatwere infused via the caudal vein 15 min before ischemia respectively and the infusion was stopped at 30 min of reperfusion, while S and M groups received equal volume of normal saline instead. Blood samples were collected from the femoral vein at 30 min and 24 h of reperfusion for measurement of serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations. The rats were sacrificed at 24 h of reperfusion and the renal tissues were removed for determination of MDA content, SOD and Ca2+ -ATPase activities. Pathological changes in renal tissues were observed with light and electron microscopes. Results Compared with group S, the concentrations of serum Cr and BUN and content of MDA were significantly increased, while activities of SOD and Ca2+ -ATPase were significantly decreased in the other 4 groups ( P ＜ 0.05 or 0.01). Compared with group M, the concentrations of serum Cr and BUN and content of MDA were significantly decreased, activities of SOD and Ca2+ -ATPase were significantly increased (P ＜0.05 or 0.01) and the pathological changes were reduced in RH, RM and RL groups. The plasma BUN and Cr concentrations and MDA content were decreased gradually and SOD and Ca2+ -ATPase activities were increased gradually with the increase in the doses of remifentanil in RL, RM and RH groups ( P ＜ 0.05 or 0.01 ).Remifentanil infusion significantly attenuated the pathologic changes in a dose-dependent manner. Conclusion Remifentanil can reduce the renal I/R injury in a dose-dependent manner by inhibiting lipid peroxidation and increasing Ca2+ -ATPase activity.