Effects of remifentanil preconditioning on renal injury induced by limb ischemia-reperfusion in rats
10.3760/cma.j.issn.0254-1416.2014.09.004
- VernacularTitle:瑞芬太尼预先给药对大鼠肢体缺血再灌注致肾损伤的影响
- Author:
Lukun YANG
;
Xueling BAI
;
Xiaoyu XIAO
;
Rongkai ZHANG
- Publication Type:Journal Article
- Keywords:
Piperidines;
Reperfusion injury;
Extremities;
Kidney
- From:
Chinese Journal of Anesthesiology
2014;34(9):1048-1050
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effects of remifentanil preconditioning on the renal injury induced by limb ischemia-reperfusion (I/R) in rats.Methods Twenty-seven healthy male Sprague-Dawley rats,weighing 200-250 g,were randomly assigned into 3 groups (n =9 each):sham operation group (Sham group),I/R group and remifentanil preconditioning group (RPC group).Limb ischemia was induced by clamping bilateral femoral arteries and veins for 2 h,followed by 24 h reperfusion in I/R and RPC groups.Remifentanil 1.0 μg· kg-1 · min-1 was infused via the caudal vein for 30 min before ischemia in RPC group,while the equal volume of normal saline was given in Sham and I/R groups.Blood sample was taken from the inferior vena cava at 24 h of reperfusion to measure blood urea nitrogen (BUN) and creatinine (Cr) concentrations in serum.The rats were sacrificed and the left kidney was removed for determination of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) contents,cell apoptosis and microscopic examination of pathological changes.Apoptosis index was calculated.Results Apoptosis index and concentrations of BUN and Cr in serum,TNF-α and IL-6 contents,and apoptosis index were significantly higher,and the pathological changes were more severe in I/R and RPC groups than in Sham group.Compared with group I/R,concentrations of BUN and Cr in serum,TNF-α and IL-6 contents,and apoptosis index were significantly decreased,and the pathological changes were attenuated in RPC group.Conclusion Remifentanil preconditioning can attenuate renal injury induced by limb I/R in rats,and inhibition of inflammatory responses and cell apoptosis in kidney may be involved in the mechanism.