Effect of sevoflurane postconditioning on renal injury induced by hind limb ischemia-reperfusion in rats
10.3760/cma.j.issn.0254-1416.2012.08.033
- VernacularTitle:七氟醚后处理对肢体缺血再灌注诱发大鼠肾损伤的影响
- Author:
Shaopeng ZHOU
;
Lukun YANG
;
Xiaoyu XIAO
;
Lu LIU
;
Hua LIU
- Publication Type:Journal Article
- Keywords:
Anesthetics,inhalation;
Extremities;
Reperfusion injury;
Kidney function tests
- From:
Chinese Journal of Anesthesiology
2012;32(8):1017-1019
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of sevoflurane postconditioning on the renal injury induced by hind limb ischemia-reperfusion (I/R) in rats.Methods Twenty-four healthy male Sprague-Dawley rats,weighing 200-250 g,were randomly assigned into 3 groups (n =8 each):sham operation group (group S),group I/R and sevoflurane group (group Spo).Limb ischemia was induced by occlusion of bilateral hind limbs for 4 h followed by 6 h reperfusion.In group Spo,sevoflurane was inhaled for 6 h at the end-tidal concentration of 2.5 ％ before reperfusion,while pure oxygen was inhaled instead of sevoflurane in groups S and I/R.Blood samples were taken from the inferior vena cava at 6 h of reperfusion to determine the serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations.The rats were then sacrificed and the kidney was removed for determination of superoxide dismutase (SOD) activity and contents of malondialdehyde (MDA),tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and for microscopic examination.Results The levels of BUN,Cr,MDA,TNF-α and IL-6 were significantly higher,the SOD content was significantly lower (P ＜ 0.05),and the pathological damage was severer in groups I/R and Spo than in group S.Compared with group I/R,the levels of BUN,Cr,MDA,TNF-α and IL-6 were significantly decreased,the SOD content was significantly increased (P ＜ 0.05),and the pathological damage was attenuated in group S.Conclusion Sevoflurane postconditioning can reduce the renal injury induced by hind limb I/R in rats,and the reduction of oxygen radical release and inhibition of inflammatory response may be involved in the mechanism.
