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本文引用的文献

1
Ischaemic conditioning strategies for the nephrologist: a promise lost in translation?肾病学家的缺血预处理策略:翻译中迷失的希望?
Nephrol Dial Transplant. 2014 Oct;29(10):1827-40. doi: 10.1093/ndt/gfu034. Epub 2014 Mar 2.
2
Ischemic preconditioning protects cardiomyocyte mitochondria through mechanisms independent of cytosol.缺血预处理通过与细胞质无关的机制保护心肌细胞线粒体。
J Mol Cell Cardiol. 2014 Mar;68:79-88. doi: 10.1016/j.yjmcc.2014.01.001. Epub 2014 Jan 13.
3
Administration of dexamethasone protects mice against ischemia/reperfusion induced renal injury by suppressing PI3K/AKT signaling.地塞米松的给药通过抑制PI3K/AKT信号传导来保护小鼠免受缺血/再灌注诱导的肾损伤。
Int J Clin Exp Pathol. 2013 Oct 15;6(11):2366-75. eCollection 2013.
4
Meta-analysis of ischaemic preconditioning for liver resections.肝切除术缺血预处理的荟萃分析。
Br J Surg. 2013 Dec;100(13):1689-700. doi: 10.1002/bjs.9277.
5
Sinomenine protects mice against ischemia reperfusion induced renal injury by attenuating inflammatory response and tubular cell apoptosis.青藤碱通过减轻炎症反应和肾小管细胞凋亡来保护小鼠免受缺血再灌注诱导的肾损伤。
Int J Clin Exp Pathol. 2013 Aug 15;6(9):1702-12. eCollection 2013.
6
Protective effect of ischemic preconditioning on ischemia/reperfusion-induced acute kidney injury through sympathetic nervous system in rats.缺血预处理通过大鼠交感神经系统对缺血/再灌注诱导的急性肾损伤的保护作用。
Eur J Pharmacol. 2013 Oct 15;718(1-3):206-12. doi: 10.1016/j.ejphar.2013.08.032. Epub 2013 Sep 12.
7
Lipopolysaccharide-induced cross-tolerance against renal ischemia-reperfusion injury is mediated by hypoxia-inducible factor-2α-regulated nitric oxide production.脂多糖诱导的肾缺血再灌注损伤交叉耐受是由缺氧诱导因子-2α调节的一氧化氮产生介导的。
Kidney Int. 2014 Feb;85(2):276-88. doi: 10.1038/ki.2013.342. Epub 2013 Sep 11.
8
Nitric oxide synthase inhibition and oxidative stress in cardiovascular diseases: possible therapeutic targets?一氧化氮合酶抑制与氧化应激在心血管疾病中的作用:可能的治疗靶点?
Pharmacol Ther. 2013 Dec;140(3):239-57. doi: 10.1016/j.pharmthera.2013.07.004. Epub 2013 Jul 13.
9
Effects of ischemic preconditioning in the late phase on homing of endothelial progenitor cells in renal ischemia/reperfusion injury.晚期缺血预处理对肾缺血/再灌注损伤中内皮祖细胞归巢的影响。
Transplant Proc. 2013 Mar;45(2):511-6. doi: 10.1016/j.transproceed.2012.05.095.
10
Ischemic preconditioning increases endothelial progenitor cell number to attenuate partial nephrectomy-induced ischemia/reperfusion injury.缺血预处理可增加内皮祖细胞数量,减轻部分肾切除术诱导的缺血/再灌注损伤。
PLoS One. 2013;8(1):e55389. doi: 10.1371/journal.pone.0055389. Epub 2013 Jan 31.

缺血预处理对肾缺血再灌注损伤中全身及肾脏血流动力学变化的影响。

Effects of ischemic preconditioning on the systemic and renal hemodynamic changes in renal ischemia reperfusion injury.

作者信息

Ge Yu-Zheng, Wu Ran, Xin Hui, Liu Hao, Lu Tian-Ze, Zhao You-Cai, Shen Jiang-Wei, Hu Zhi-Kai, Yu Peng, Zhou Liu-Hua, Xu Lu-Wei, Xu Zheng, Wu Jian-Ping, Li Wen-Cheng, Zhu Jia-Geng, Jia Rui-Peng

机构信息

Department of Urology, Nanjing First Hospital, Nanjing Medical University 68 Changle Road, Nanjing 210006, China ; Center for Renal Transplantation, Nanjing First Hospital, Nanjing Medical University 68 Changle Road, Nanjing 210006, China.

Department of Urology, The Second Affiliated Hospital of Zhejiang University School of Medicine 88 Jiefang Road, Hangzhou 310009, China.

出版信息

Int J Clin Exp Pathol. 2015 Feb 1;8(2):1128-40. eCollection 2015.

PMID:25972999
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4396246/
Abstract

BACKGROUND

Ischemic preconditioning (IPC) could protect against subsequent renal ischemia reperfusion injury (IRI). However, the mechanisms underlying IPC remain far from complete. Hence, we explored the effects of IPC on the renal and systemic hemodynamic changes, renal function and morphology, as well the involvement of endothelial and inducible nitric oxide synthase (eNOS/iNOS), and nitric oxide (NO).

METHODS

Male Sprague-Dawley rats were randomly divided into five groups after right-side nephrectomy: Sham group (surgery without vascular clamping); IRI group (the left renal artery was clamped for 45 min); IPC group (pretreated with 15 min of ischemia and 10 min of reperfusion); IPC + vehicle group (administrated with 0.9% saline 5 min before IPC); and IPC + N(G)-nitro-L-arginine methylester (L-NAME) group (pretreated with L-NAME 5 min prior to IPC). The renal and systemic hemodynamic parameters, renal function and morphology, as well as eNOS, iNOS, and NO expression levels in the kidneys were measured at the indicated time points after reperfusion.

RESULTS

IPC rats exhibited significant improvements in renal function, morphology, and renal artery blood flow (RABF), without obvious influence on the systemic hemodynamics and renal vein blood flow. Increased eNOS, iNOS, and NO expression levels were detected in the kidneys of IPC rats 24 h after reperfusion. Furthermore, the beneficial effects were fully abolished by the administration of L-NAME.

CONCLUSIONS

The results suggest that IPC contributes to early restoration of RABF, probably through eNOS/iNOS-mediated NO production, thereby alleviating the renal dysfunction and histological damage caused by IRI.

摘要

背景

缺血预处理(IPC)可预防随后的肾缺血再灌注损伤(IRI)。然而,IPC的潜在机制仍远未完全明确。因此,我们探讨了IPC对肾脏和全身血流动力学变化、肾功能和形态的影响,以及内皮型和诱导型一氧化氮合酶(eNOS/iNOS)和一氧化氮(NO)的作用。

方法

雄性Sprague-Dawley大鼠在右侧肾切除术后随机分为五组:假手术组(手术但不夹闭血管);IRI组(左肾动脉夹闭45分钟);IPC组(预处理15分钟缺血和10分钟再灌注);IPC + 溶媒组(IPC前5分钟给予0.9%生理盐水);IPC + N(G)-硝基-L-精氨酸甲酯(L-NAME)组(IPC前5分钟用L-NAME预处理)。在再灌注后的指定时间点测量肾脏和全身血流动力学参数、肾功能和形态,以及肾脏中eNOS、iNOS和NO的表达水平。

结果

IPC组大鼠的肾功能、形态和肾动脉血流量(RABF)有显著改善,对全身血流动力学和肾静脉血流量无明显影响。再灌注24小时后,IPC组大鼠肾脏中eNOS、iNOS和NO的表达水平升高。此外,给予L-NAME可完全消除这些有益作用。

结论

结果表明,IPC可能通过eNOS/iNOS介导的NO生成促进RABF的早期恢复,从而减轻IRI所致的肾功能障碍和组织学损伤。