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缺氧和再灌注后联合心脏骤停和心肺复苏的中枢神经组织损伤:作用机制和缓解可能性。

Central nervous tissue damage after hypoxia and reperfusion in conjunction with cardiac arrest and cardiopulmonary resuscitation: mechanisms of action and possibilities for mitigation.

机构信息

Laboratory of Cerebrovascular Research, Department of Surgical Sciences, Anesthesiology & Intensive Care Medicine, University Hospital, Uppsala University, Uppsala, Sweden.

出版信息

Int Rev Neurobiol. 2012;102:173-87. doi: 10.1016/B978-0-12-386986-9.00007-7.

Abstract

Only approximately 10% of patients encountering a cardiac arrest (CA) and subsequent cardiopulmonary resuscitation survive to a meaningful life. One of the most important causes for this low survival rate is the ischemia-reperfusion injury that hits the brain. This review summarizes some of the more important mechanisms causing cerebral injury. Thus, we describe some of our findings when performing genome-wide transcriptional profiling as well as histological and immunohistological staining of cerebral cortical areas. In order to shed some light on therapeutic opportunities, our findings relating to the use of induced mild hypothermia and methylene blue as neuroprotective agents are reviewed. Furthermore, we would like to share some interesting data on gender differences and effects of estrogen on the ensuing cerebral injury occurring after hypovolemic CA.

摘要

只有大约 10%遭遇心脏骤停(CA)和随后心肺复苏的患者能够存活并过上有意义的生活。造成这种低存活率的最重要原因之一是大脑受到的缺血再灌注损伤。本综述总结了导致脑损伤的一些更重要的机制。因此,我们描述了在进行全基因组转录谱分析以及大脑皮质区域的组织学和免疫组织化学染色时的一些发现。为了揭示治疗机会,我们回顾了使用诱导性轻度低温和亚甲蓝作为神经保护剂的发现。此外,我们还想分享一些关于性别差异和雌激素对出血性 CA 后继发脑损伤影响的有趣数据。

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