de Resende Marco A C, Pantoja Alberto V, Barcellos Bruno M, Reis Eduardo P, Consolo Thays D, Módolo Renata P, Domingues Maria A C, Assad Alexandra R, Cavalcanti Ismar L, Castiglia Yara M M, Módolo Norma S P
Pós-Graduação em Anestesiologia, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista (UNESP), 18618-970 Botucatu, SP, Brazil ; Serviço de Anestesiologia, Departamento de Cirurgia, Universidade Federal Fluminense (UFF), 24033-900 Niterói, RJ, Brazil.
Serviço de Anestesiologia, Departamento de Cirurgia, Universidade Federal Fluminense (UFF), 24033-900 Niterói, RJ, Brazil.
Biomed Res Int. 2015;2015:864902. doi: 10.1155/2015/864902. Epub 2015 Aug 27.
Ischemic postconditioning (IP) in renal Ischemia reperfusion injury (IRI) models improves renal function after IRI. Ketamine affords significant benefits against IRI-induced acute kidney injury (AKI). The present study investigated the effects of IP and IP associated with subanesthetic S(+)-ketamine in ischemia-reperfusion-induced AKI.
Forty-one Wistar rats were randomized into four groups: CG (10), control; KG (10), S(+)-ketamine infusion; IPG (10), IP; and KIPG (11), S(+)-ketamine infusion + IP. All rats underwent right nephrectomy. IRI and IP were induced only in IPG and KIPG by left kidney arterial occlusion for 30 min followed by reperfusion for 24 h. Complete reperfusion was preceded by three cycles of 2 min of reocclusion followed by 2 min of reperfusion. Renal function was assessed by measuring serum neutrophil gelatinase-associated lipocalin (NGAL), creatinine, and blood urea nitrogen (BUN). Tubular damage was evaluated by renal histology.
Creatinine and BUN were significantly increased. Severe tubular injury was only observed in the groups with IRI (IPG and KIPG), whereas no injury was observed in CG or KG. No significant differences were detected between IPG and KIPG.
No synergic effect of the use of subanesthetic S(+)-ketamine and IP on AKI was observed in this rat model.
在肾缺血再灌注损伤(IRI)模型中,缺血后处理(IP)可改善IRI后的肾功能。氯胺酮对IRI诱导的急性肾损伤(AKI)有显著益处。本研究调查了IP以及与亚麻醉剂量S(+)-氯胺酮联合应用的IP在缺血再灌注诱导的AKI中的作用。
41只Wistar大鼠被随机分为四组:CG组(10只),对照组;KG组(10只),输注S(+)-氯胺酮;IPG组(10只),IP组;KIPG组(11只),输注S(+)-氯胺酮+IP组。所有大鼠均行右肾切除术。仅在IPG组和KIPG组通过左肾动脉阻断30分钟,然后再灌注24小时诱导IRI和IP。在完全再灌注之前,进行三个循环的再阻断2分钟,然后再灌注2分钟。通过测量血清中性粒细胞明胶酶相关脂质运载蛋白(NGAL)、肌酐和血尿素氮(BUN)评估肾功能。通过肾脏组织学评估肾小管损伤。
肌酐和BUN显著升高。仅在IRI组(IPG组和KIPG组)观察到严重的肾小管损伤,而在CG组或KG组未观察到损伤。IPG组和KIPG组之间未检测到显著差异。
在该大鼠模型中,未观察到亚麻醉剂量S(+)-氯胺酮与IP联合应用对AKI有协同作用。