机制(生物学)
缺血
肾
再灌注损伤
医学
心脏病学
内科学
哲学
认识论
出处
期刊:生物物理学
[Hans Publishers]
日期:2016-01-01
卷期号:04 (03): 19-29
标识
DOI:10.12677/jps.2016.43003
摘要
缺血再灌注损伤(IRI)是指在缺血的基础上恢复血流后组织损伤反而加重的现象。肾脏缺血再灌注损伤引起的急性肾功能损伤(AKI)在临床上具有很高的死亡率。其机制非常复杂,涉及多种因素共同作用,且目前对于IRI的具体作用机制尚不十分明确,目前认为与缺血再灌注后的炎症反应、氧化应激、细胞内钙超载、肾素-血管紧张素激活、微循环障碍等有关。更好的理解肾缺血再灌注损伤的机制才能找到有效的防治措施。这篇综述我们总结了缺血再灌注损伤可能的机制及防治措施。 Ischemia-reperfusion injury (IRI) occurs when the blood flow to the particular organ is ob-structed, followed by the restoration of blood to the ischemic organ. In the kidney, IRI contributes to pathological conditions called acute kidney injury (AKI) that is a clinical syndrome with rapid kidney dysfunction and high mortality rates. Although the pathophysiology of IRI is very complicated and is not completely understood, several important mechanisms resulting in kidney failure have been mentioned. IRI usually is associated with an inflammatory reaction, oxidative stress, intracellular Ca2+ overload, renin-angiotensin activation and microcirculation disturbance. Better understanding of the cellular pathophysiological mechanisms underlying kidney injury will hope- fully result in the design of more targeted therapies to prevent and treat the injury. In this review, we summarize some important potential mechanisms and therapeutic approaches in renal IRI.
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