Subarachnoid hemorrhage, spreading depolarizations and impaired neurovascular coupling.

Subarachnoid hemorrhage, spreading depolarizations and impaired neurovascular coupling.
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DOI:
10.1155/2013/819340
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发表时间:
2013
影响因子:
1.5
通讯作者:
Wellman GC
Wellman GC
中科院分区:
其他
文献类型:
--
作者:
Koide M;Sukhotinsky I;Ayata C;Wellman GC

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动脉瘤性蛛网膜下腔出血(SAH)严重影响脑功能,严重影响神经元与血管之间的通讯,导致脑缺血。从生理上讲,神经血管偶联是指大脑血流量的局部增加,以满足大脑活跃区域内神经元代谢需求的增加。神经血管偶联是一个持续的过程,涉及神经血管单位-神经元、星形胶质细胞和实质小动脉的协调活动。神经元活动也可以在更大范围内影响脑血流。扩散性去极化(SD)是神经元去极化的自传播波,可在偏头痛、创伤性脑损伤和中风时观察到。通常,SD与脑血流量增加有关。新的证据表明,SAH导致局部和全球水平的神经血管沟通倒置。与其他导致SD的事件不同,SAH诱导的SD减少而不是增加脑血流量。此外,在神经血管单位的水平上,SAH引起神经血管偶联从血管扩张到血管收缩的倒置。全球缺血也会对神经血管反应产生不利影响。在这里,我们总结了关于SAH和全脑缺血对神经血管通讯的影响的现有知识。对这些事件的机械性理解应该为治疗这些神经血管疾病提供新的策略。
Aneurysmal subarachnoid hemorrhage (SAH) has devastating consequences on brain function including profound effects on communication between neurons and the vasculature leading to cerebral ischemia. Physiologically, neurovascular coupling represents a focal increase in cerebral blood flow to meet increased metabolic demand of neurons within active regions of the brain. Neurovascular coupling is an ongoing process involving coordinated activity of the neurovascular unit—neurons, astrocytes, and parenchymal arterioles. Neuronal activity can also influence cerebral blood flow on a larger scale. Spreading depolarizations (SD) are self-propagating waves of neuronal depolarization and are observed during migraine, traumatic brain injury, and stroke. Typically, SD is associated with increased cerebral blood flow. Emerging evidence indicates that SAH causes inversion of neurovascular communication on both the local and global level. In contrast to other events causing SD, SAH-induced SD decreases rather than increases cerebral blood flow. Further, at the level of the neurovascular unit, SAH causes an inversion of neurovascular coupling from vasodilation to vasoconstriction. Global ischemia can also adversely affect the neurovascular response. Here, we summarize current knowledge regarding the impact of SAH and global ischemia on neurovascular communication. A mechanistic understanding of these events should provide novel strategies to treat these neurovascular disorders.