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实验性蛛网膜下腔出血的进展

Advances in experimental subarachnoid hemorrhage.

作者信息

Zhou Yilin, Martin Robert D, Zhang John H

机构信息

Department of Anesthesiology, Loma Linda University School of Medicine, Loma Linda, CA 92354, USA.

出版信息

Acta Neurochir Suppl. 2011;110(Pt 1):15-21. doi: 10.1007/978-3-7091-0353-1_3.

Abstract

Subarachnoid hemorrhage (SAH) remains to be a devastating disease with high mortality and morbidity. Two major areas are becoming the focus of the research interest of SAH: these are cerebral vasospasm (CVS) and early brain injury (EBI). This mini review will provide a broad summary of the major advances in experimental SAH during the last 3 years. Treatments interfering with nitric oxide (NO)- or endothelin-pathways continue to show antispasmotic effects in experimental SAH. HIF 1 may play both a detrimental and beneficial role in the setting of SAH, depending on its activation stage. Inflammation and oxidative stress contribute to the pathophysiology of both CVS and EBI. Apoptosis, a major component of EBI after SAH, also underlie the etiology of CVS. Since we recognize now that CVS and EBI are the two major contributors to the significant mortality and morbidity associated with SAH, ongoing research will continue to elucidate the underlying pathophysiological pathways and treatment strategies targeting both CVS and EBI may be more successful and improve outcome of patients with SAH.

摘要

蛛网膜下腔出血(SAH)仍然是一种具有高死亡率和高发病率的毁灭性疾病。两个主要领域正成为SAH研究兴趣的焦点:即脑血管痉挛(CVS)和早期脑损伤(EBI)。本综述将对过去3年实验性SAH的主要进展进行广泛总结。干扰一氧化氮(NO)或内皮素途径的治疗在实验性SAH中继续显示出抗痉挛作用。缺氧诱导因子1(HIF 1)在SAH情况下可能发挥有害和有益的作用,这取决于其激活阶段。炎症和氧化应激促成了CVS和EBI的病理生理学。凋亡是SAH后EBI的主要组成部分,也是CVS病因的基础。由于我们现在认识到CVS和EBI是与SAH相关的高死亡率和高发病率的两个主要因素,正在进行的研究将继续阐明潜在的病理生理途径,针对CVS和EBI的治疗策略可能会更成功,并改善SAH患者的预后。

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