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缺血性脑损伤机制的不断变化态势。

The changing landscape of ischaemic brain injury mechanisms.

作者信息

Lee J M, Zipfel G J, Choi D W

机构信息

Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, Saint Louis, Missouri 63110, USA.

出版信息

Nature. 1999 Jun 24;399(6738 Suppl):A7-14. doi: 10.1038/399a007.

DOI:10.1038/399a007
PMID:10392575
Abstract

Thrombolysis has become established as an acute treatment for human stroke. But despite multiple clinical trials, neuroprotective strategies have yet to be proved effective in humans. Here we discuss intrinsic tissue mechanisms of ischaemic brain injury, and present a perspective that broadening of therapeutic targeting beyond excitotoxicity and neuronal calcium overload will be desirable for developing the most effective neuroprotective therapies.

摘要

溶栓已成为治疗人类中风的一种急性疗法。但尽管进行了多项临床试验,神经保护策略在人类中尚未被证明有效。在此,我们讨论缺血性脑损伤的内在组织机制,并提出一种观点,即对于开发最有效的神经保护疗法而言,将治疗靶点拓宽至兴奋性毒性和神经元钙超载之外是可取的。

相似文献

1
The changing landscape of ischaemic brain injury mechanisms.缺血性脑损伤机制的不断变化态势。
Nature. 1999 Jun 24;399(6738 Suppl):A7-14. doi: 10.1038/399a007.
2
[Glutamate neurotransmission and calcium metabolism in cerebral ischaemia and under normal conditions].[脑缺血及正常条件下的谷氨酸神经传递与钙代谢]
Usp Fiziol Nauk. 2002 Oct-Dec;33(4):80-93.
3
Trial design and reporting standards for intra-arterial cerebral thrombolysis for acute ischemic stroke.急性缺血性脑卒中动脉内脑溶栓的试验设计与报告标准。
Stroke. 2003 Aug;34(8):e109-37. doi: 10.1161/01.STR.0000082721.62796.09. Epub 2003 Jul 17.
4
Possible mechanisms limiting N-methyl-D-aspartate receptor overactivation and the therapeutic efficacy of N-methyl-D-aspartate antagonists.限制N-甲基-D-天冬氨酸受体过度激活的可能机制及N-甲基-D-天冬氨酸拮抗剂的治疗效果。
Stroke. 1990 Nov;21(11 Suppl):III20-2.
5
[Reperfusion in acute ischaemic stroke: present and future].[急性缺血性卒中的再灌注治疗:现状与未来]
An Sist Sanit Navar. 2008;31 Suppl 1:31-46.
6
Role of nonsynaptic GluN2B-containing NMDA receptors in excitotoxicity: evidence that fluoxetine selectively inhibits these receptors and may have neuroprotective effects.非突触 GluN2B 型 NMDA 受体在兴奋性毒性中的作用:氟西汀选择性抑制这些受体并可能具有神经保护作用的证据。
Brain Res Bull. 2013 Apr;93:32-8. doi: 10.1016/j.brainresbull.2012.10.005. Epub 2012 Oct 23.
7
Evolving therapeutic approaches to treating acute ischemic stroke.治疗急性缺血性中风的不断发展的治疗方法。
J Neurol Sci. 2006 Nov 15;249(2):101-9. doi: 10.1016/j.jns.2006.06.010. Epub 2006 Sep 26.
8
Potassium channel blockers attenuate hypoxia- and ischemia-induced neuronal death in vitro and in vivo.钾通道阻滞剂在体外和体内均能减轻缺氧和缺血诱导的神经元死亡。
Stroke. 2003 May;34(5):1281-6. doi: 10.1161/01.STR.0000065828.18661.FE. Epub 2003 Apr 3.
9
[Pathological role of intracellular calcium overload in ischemic neuronal death].细胞内钙超载在缺血性神经元死亡中的病理作用
Tanpakushitsu Kakusan Koso. 1998 Sep;43(12 Suppl):1884-90.
10
[Mechanisms of brain tissue damage in acute focal cerebral ischemia].[急性局灶性脑缺血中脑组织损伤的机制]
Zh Nevrol Psikhiatr Im S S Korsakova. 1999;99(2):65-70.

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Glutamate acts on acid-sensing ion channels to worsen ischaemic brain injury.谷氨酸通过酸感应离子通道作用导致缺血性脑损伤加重。
Nature. 2024 Jul;631(8022):826-834. doi: 10.1038/s41586-024-07684-7. Epub 2024 Jul 10.
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