Effects of ketamine on renal ischemia-reperfusion injury in rats
10.3760/cma.j.issn.0254-1416.2009.10.016
- VernacularTitle:氯胺酮对大鼠肾脏缺血再灌注损伤的影响
- Author:
Aijun YAO
;
Yufang LENG
- Publication Type:Journal Article
- Keywords:
Ketamine;
Reperfusion injury;
Kindey;
Apoptosis
- From:
Chinese Journal of Anesthesiology
2009;29(10):927-931
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of ketamine on the renal ischemia-reperfusion (IR) injury in rats and the underlying mechanism. Methods Twenty-four male Wistur rats weighing 220-250 g were randomly divided into 4 groups (n=6 each): sham operation group (group S), IR group, ketumine 2 mg/kg group (group K_1), ketamine 10 mg/kg group (group K_2). The rats were anesthetized with intraperitoneal chloral hydrate 300 mg/kg. Renal ischemia was induced by clamping the left renal artery for 45 min followed by 6 h of repednsion using an atraumatic clamp. In group K_1 and K_2, ketaminc 2 and 10 mg/kg were injected via the caudal vein 5 min before the repedusion respectively. The rats were killed at 6 h of reperfusion, and blood samples were collected from the right auricle for measurement of serum creatiniue (Cr) and blood urea nitrogen (BUN) concentrations. Pathological changes in renal tissues were observed with light and electron microscopes. The expression of Fas and Caspsse-3 in the renal tubular epithelial cell was determined by immuno-histochemistry. The apeptosis in the renal tubular epithelial cell was detected by TUNEL assay. Apeptotic index (AI) was calculated. Results Compared with group S, the levels of serum Cr and BUN, expression of Fas and Caspase-3 and AI were significantly increased in group IR, K_1 and K_2 (P < 0.01). The levels of serum Cr and BUN, expression of Fas and Caspase-3 and AI were significantly lower in group K_(1,2) than in group IR and in group K2 than in group K_1 (P<0.01). The microscopic examination showed that the renal IR injury was obviously attenuated in group K_2 compared with group K_1. Conclusion Ketamine can attenuate the renal injury induced by IR in a dose-dependent manner in rats. The underlying mechanism may be related to the inhibition of apoptosis in the renal tubular epithelial cell.
