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在大鼠肾脏中,瑞芬太尼在减轻肾缺血再灌注损伤方面是否比右美托咪定更有效?

Does remifentanil attenuate renal ischemia-reperfusion injury better than dexmedetomidine in rat kidney?

作者信息

Erkılıç E, Kesimci E, Alaybeyoğlu F, Kılınç I, Tural R, Yazgan A, Gümüş T, Sepici Dinçel A, Dumlu E G, Kanbak O

机构信息

Anesthesiology and Reanimation Department.

General Surgery Department, Atatürk Training and Research Hospital.

出版信息

Drug Des Devel Ther. 2017 Mar 8;11:677-683. doi: 10.2147/DDDT.S126701. eCollection 2017.

DOI:10.2147/DDDT.S126701
PMID:28331287
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5352155/
Abstract

BACKGROUND

Ischemia-reperfusion (I/R) injury is a common cause of patient morbidity and mortality in the perioperative period. Patients undergoing long-lasting, abdominal, and urogenital surgeries with risk factors such as advanced age, peripheral artery disease, diabetes mellitus, renovascular disease, and congestive heart failure are candidates for acute kidney injury (AKI) due to impaired renal perfusion and decreased functional renal reserve. Pharmacological agents with multiple functions and anti-oxidative and anti-inflammation properties may be promising preventative strategies for AKI. Recently, dexmedetomidine (dex) has been postulated to have renoprotective effects.

OBJECTIVES

We aimed to investigate the protective effects of an intravenous anesthetic remifentanil in renal I/R injury in the rat in comparison with dex.

MATERIALS AND METHODS

A total of 30 Sprague Dawley adult rats were randomly assigned into five groups: the control group (group C, n=6), the sham group (group Sh, n=6, saline-infused rats without I/R injury), the saline group (group S, n=6, saline-infused rats with I/R injury), the remifentanil-treated group (group REM, n=6), and the dexmedetomidine-treated group (group DEX, n=6). The infusions (saline, remifentanil, and dex) were started after anesthesia induction and right nephrectomy and continued until the end of the surgical procedure. In I/R injury groups, the left renal artery and vein were occluded together by a clamp for 30 minutes and reperfusion lasted for 30 minutes. The rats were sacrificed after reperfusion, and the left kidney tissue was harvested. Blood samples were drawn from all animals to evaluate plasma neutrophil gelatinase-associated lipocalin (NGAL) at the beginning, 15 minutes after ischemia, 15 minutes after reperfusion, and 6 hours after the surgical procedure (T0, T1, T2, and T3, respectively).

RESULTS

The plasma NGAL levels exhibited increase at T1, T2, and T3 compared to the levels at T0 in group S (<0.05). In group REM, there was a significant increase in plasma NGAL levels at T3 in comparison to those at T0, T1, and T2. The plasma NGAL levels at T2 in group S were significantly higher than those at T2 in group DEX (<0.05). The groups S and REM showed significantly higher plasma NGAL levels at T3 compared to those at T0 (<0.05). Upon histological examination, there was no difference among the study groups when left kidneys were evaluated (>0.05).

CONCLUSION

The NGAL levels and histopathological findings reflected protection by dex against renal I/R injury. However, the same exact results could not be mentioned for remifentanil depending on our study results.

摘要

背景

缺血再灌注(I/R)损伤是围手术期患者发病和死亡的常见原因。接受长时间腹部和泌尿生殖系统手术且伴有高龄、外周动脉疾病、糖尿病、肾血管疾病和充血性心力衰竭等危险因素的患者,由于肾灌注受损和功能性肾储备减少,是急性肾损伤(AKI)的候选者。具有多种功能以及抗氧化和抗炎特性的药物可能是预防AKI的有前景的策略。最近,右美托咪定(dex)被认为具有肾脏保护作用。

目的

我们旨在研究静脉麻醉药瑞芬太尼与右美托咪定相比,对大鼠肾I/R损伤的保护作用。

材料与方法

总共30只成年Sprague Dawley大鼠随机分为五组:对照组(C组,n = 6)、假手术组(Sh组,n = 6,输注生理盐水且无I/R损伤的大鼠)、生理盐水组(S组,n = 6,输注生理盐水且有I/R损伤的大鼠)、瑞芬太尼治疗组(REM组,n = 6)和右美托咪定治疗组(DEX组,n = 6)。在麻醉诱导和右肾切除术后开始输注(生理盐水、瑞芬太尼和右美托咪定),并持续至手术结束。在I/R损伤组中,用血管夹同时夹闭左肾动脉和静脉30分钟,再灌注持续30分钟。再灌注后处死大鼠,获取左肾组织。在开始时、缺血15分钟后、再灌注15分钟后以及手术后6小时(分别为T0、T1、T2和T3)从所有动物采集血样,以评估血浆中性粒细胞明胶酶相关脂质运载蛋白(NGAL)。

结果

与S组T0时的水平相比,S组在T1、T2和T3时血浆NGAL水平升高(<0.05)。在REM组中,与T0、T1和T2时相比,T3时血浆NGAL水平显著升高。S组T2时的血浆NGAL水平显著高于DEX组T2时的水平(<0.05)。与T0时相比,S组和REM组在T3时的血浆NGAL水平显著更高(<0.05)。组织学检查时,评估左肾时各研究组之间无差异(>0.05)。

结论

NGAL水平和组织病理学结果反映了右美托咪定对肾I/R损伤的保护作用。然而,根据我们的研究结果,瑞芬太尼的情况并非如此。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/88ce82d09084/dddt-11-677Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/d117e6689ab1/dddt-11-677Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/1987c87da6c3/dddt-11-677Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/87df840fc119/dddt-11-677Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/0d9fca2aeaa0/dddt-11-677Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/88ce82d09084/dddt-11-677Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/d117e6689ab1/dddt-11-677Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/1987c87da6c3/dddt-11-677Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/87df840fc119/dddt-11-677Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/0d9fca2aeaa0/dddt-11-677Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e41/5352155/88ce82d09084/dddt-11-677Fig5.jpg

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