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高压氧治疗可保护肾脏免受缺血再灌注损伤。

Hyperbaric oxygenation protects the kidney against ischemia-reperfusion injury.

机构信息

Department of Cardiovascular Physiology, Institute for Medical Research, University of Belgrade, Belgrade, Serbia.

Institute of Medical Physiology, School of Medicine, University of Belgrade, Belgrade Serbia.

出版信息

Undersea Hyperb Med. 2020 First Quarter;47(1):21-30. doi: 10.22462/01.03.2020.3.


DOI:10.22462/01.03.2020.3
PMID:32176943
Abstract

BACKGROUND: Acute kidney injury (AKI) as a consequence of ischemia is a common clinical event that can lead to unacceptably high morbidity and mortality. Hyperbaric oxygen (HBO2) preconditioning has been shown to prevent ischemia-reperfusion injury (IRI) in different tissues. OBJECTIVES: The aim of our study was to compare the effects of HBO2 preconditioning on renal hemodynamics, kidney function and oxidative stress in normotensive and spontaneously hypertensive rats that suffered kidney IRI. METHODS: An experiment was performed on Wistar (normotensive) and spontaneously hypertensive rats (SHR). The animals were divided into the following experimental groups: sham-operated rats and rats with or without HBO2 preconditioning 24 hours before post-ischemic AKI induction. Treated rats were placed into experimental HBO2 chambers and exposed to pure oxygen twice a day for two consecutive days (2.026 bar of oxygen) for 60 minutes. AKI was performed the next morning. The right kidney was removed and the renal ischemia was performed by clamping the left renal artery for 45 minutes. RESULTS: In this study, HBO2 preconditioning significantly improved disturbed renal hemodynamics, major markers of kidney function in plasma (creatinine, urea and phosphate) as well as antioxidant enzymes (superoxide dismutase and catalase) activities in erythrocytes after AKI induction. Also, HBO2 preconditioning decreased lipid peroxidation in plasma after ischemic AKI. Positive effects were observed in both strains of rats. CONCLUSIONS: Our results suggest that HBO2 treatment improves renal hemodynamic and kidney function and decreases oxidative stress of Wistar and SHR rats with an AKI episode. Furthermore, it also implies that pre-existing hypertension does not affect the beneficial effects of HBO2 preconditioning.

摘要

背景:缺血引起的急性肾损伤(AKI)是一种常见的临床事件,可导致不可接受的高发病率和死亡率。高压氧(HBO2)预处理已被证明可预防不同组织的缺血再灌注损伤(IRI)。

目的:我们的研究目的是比较 HBO2 预处理对患有肾 IRI 的正常血压和自发性高血压大鼠的肾脏血液动力学、肾功能和氧化应激的影响。

方法:在 Wistar(正常血压)和自发性高血压大鼠(SHR)上进行了一项实验。将动物分为以下实验组:假手术大鼠和缺血后 AKI 诱导前 24 小时接受或不接受 HBO2 预处理的大鼠。处理后的大鼠被放入实验性 HBO2 室中,每天两次暴露于纯氧中,持续 60 分钟,连续两天(氧 2.026 巴)。第二天早上进行 AKI。夹闭左肾动脉 45 分钟以切除右肾并进行肾缺血。

结果:在这项研究中,HBO2 预处理可显著改善 AKI 诱导后肾脏血液动力学、血浆中肾脏功能的主要标志物(肌酐、尿素和磷酸盐)以及红细胞中的抗氧化酶(超氧化物歧化酶和过氧化氢酶)活性的紊乱。此外,HBO2 预处理还可减少缺血性 AKI 后血浆中的脂质过氧化。在两种大鼠中均观察到了积极的效果。

结论:我们的结果表明,HBO2 治疗可改善 Wistar 和 SHR 大鼠 AKI 发作时的肾脏血液动力学和肾功能,并降低氧化应激。此外,这还意味着预先存在的高血压并不影响 HBO2 预处理的有益效果。

相似文献

[1]
Hyperbaric oxygenation protects the kidney against ischemia-reperfusion injury.

Undersea Hyperb Med. 2020

[2]
Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury.

Int J Mol Sci. 2021-1-30

[3]
Hyperbaric oxygen preconditioning and the role of NADPH oxidase inhibition in postischemic acute kidney injury induced in spontaneously hypertensive rats.

PLoS One. 2020-1-8

[4]
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Int J Mol Sci. 2024-3-30

[5]
Hyperoxia-induced preconditioning against renal ischemic injury is mediated by reactive oxygen species but not related to heat shock proteins 70 and 32.

Surgery. 2015-6

[6]
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[7]
Effects of Ischemic Preconditioning and Postconditioning in a Renal Ischemia-Reperfusion Injury Model: A Comparative Experimental Study in Rats.

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[8]
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[9]
Hyperbaric oxygen therapy induces kidney protection in an ischemia/reperfusion model in rats.

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[10]
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引用本文的文献

[1]
Plasma Proteomics-Based Discovery of Mechanistic Biomarkers of Hyperbaric Stress and Pulmonary Oxygen Toxicity.

Metabolites. 2023-8-23

[2]
Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury.

Int J Mol Sci. 2021-1-30

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