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持续输注右美托咪定可改善大鼠肾脏的肾缺血再灌注损伤。

Continuous infusion of dexmedetomidine improves renal ischemia-reperfusion injury in rat kidney.

作者信息

Sugita Shinji, Okabe Tadashi, Sakamoto Atsuhiro

机构信息

Department of Anesthesiology, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.

出版信息

J Nippon Med Sch. 2013;80(2):131-9. doi: 10.1272/jnms.80.131.

Abstract

BACKGROUND

Dexmedetomidine has shown beneficial effects in several inflammatory models, including ischemia-reperfusion injury (IRI). This study investigated whether the continuous infusion of dexmedetomidine could improve renal IRI in rats.

METHODS

Rats were subjected to either a sham operation and given pentobarbital (10 mg/kg/h; n=6) or were subjected to 45 minutes of renal ischemia and anesthetized with pentobarbital (10 mg/kg/h; n=6), dexmedetomidine (10 or 20 μg/kg/h; both n=6), or both pentobarbital (10 mg/kg/h) and dexmedetomidine (1.0 μg/kg/h; n=6) for 6 hours of reperfusion. Blood urea nitrogen and serum creatinine were measured 6 hours after reperfusion. Gene expression mediated by inflammatory systems in the kidney was measured with the real-time reverse-transcriptase polymerase chain reaction.

RESULTS

Treatment with 10 or 20 μg/kg/h of dexmedetomidine reduced renal dysfunction. The increases in the messenger RNA expression of interleukin-6, intercellular adhesion molecule 1, and inducible nitric oxide synthase caused by renal IRI were suppressed. Under In rats under pentobarbital anesthesia, 1.0 μg/kg/h of dexmedetomidine also improved renal dysfunction after renal IRI.

CONCLUSION

The present study demonstrates that continuous infusion of dexmedetomidine improves renal IRI. Moreover, with pentobarbital anesthesia, a dose of dexmedetomidine lower than the sedative dose also improves renal IRI.

摘要

背景

右美托咪定在包括缺血再灌注损伤(IRI)在内的多种炎症模型中已显示出有益作用。本研究调查了持续输注右美托咪定是否能改善大鼠肾IRI。

方法

将大鼠分为两组,一组进行假手术并给予戊巴比妥(10mg/kg/h;n = 6),另一组进行45分钟的肾缺血,然后用戊巴比妥(10mg/kg/h;n = 6)、右美托咪定(10或20μg/kg/h;两组n = 6)或戊巴比妥(10mg/kg/h)与右美托咪定(1.0μg/kg/h;n = 6)麻醉,再灌注6小时。再灌注6小时后测量血尿素氮和血清肌酐。用实时逆转录聚合酶链反应测量肾脏中炎症系统介导的基因表达。

结果

10或20μg/kg/h的右美托咪定治疗可减轻肾功能障碍。肾IRI引起的白细胞介素-6、细胞间黏附分子1和诱导型一氧化氮合酶信使核糖核酸表达的增加受到抑制。在戊巴比妥麻醉的大鼠中,1.0μg/kg/h的右美托咪定也可改善肾IRI后的肾功能障碍。

结论

本研究表明持续输注右美托咪定可改善肾IRI。此外,在戊巴比妥麻醉下,低于镇静剂量的右美托咪定也可改善肾IRI。

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