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本文引用的文献

1
Hypertension: a harbinger of stroke and dementia.高血压:中风和痴呆的先兆。
Hypertension. 2013 Nov;62(5):810-7. doi: 10.1161/HYPERTENSIONAHA.113.01063. Epub 2013 Aug 26.
2
Cerebral blood flow modulation by Basal forebrain or whisker stimulation can occur independently of large cytosolic Ca2+ signaling in astrocytes.基底前脑或胡须刺激可独立于星形胶质细胞中大胞浆 Ca2+信号调节脑血流。
PLoS One. 2013 Jun 13;8(6):e66525. doi: 10.1371/journal.pone.0066525. Print 2013.
3
The cortical angiome: an interconnected vascular network with noncolumnar patterns of blood flow.皮质血管网:一种具有非柱状血流模式的相互连通的血管网络。
Nat Neurosci. 2013 Jul;16(7):889-97. doi: 10.1038/nn.3426. Epub 2013 Jun 9.
4
Multimodal imaging in rats reveals impaired neurovascular coupling in sustained hypertension.多模态成像技术在大鼠中揭示了持续性高血压中的神经血管耦联受损。
Stroke. 2013 Jul;44(7):1957-64. doi: 10.1161/STROKEAHA.111.000185. Epub 2013 Jun 4.
5
The effects of hypertension on the cerebral circulation.高血压对脑循环的影响。
Am J Physiol Heart Circ Physiol. 2013 Jun 15;304(12):H1598-614. doi: 10.1152/ajpheart.00490.2012. Epub 2013 Apr 12.
6
Does stroke subtype and measurement technique influence estimation of cerebral autoregulation in acute ischaemic stroke?卒中型和测量技术是否影响急性缺血性脑卒中脑自动调节的评估?
Cerebrovasc Dis. 2013;35(3):257-61. doi: 10.1159/000347075. Epub 2013 Mar 26.
7
Intensive blood pressure lowering increases cerebral blood flow in older subjects with hypertension.强化降压增加老年高血压患者的脑血流。
Hypertension. 2013 Jun;61(6):1309-15. doi: 10.1161/HYPERTENSIONAHA.112.200972. Epub 2013 Mar 25.
8
Prostaglandin E2, a postulated astrocyte-derived neurovascular coupling agent, constricts rather than dilates parenchymal arterioles.前列腺素 E2,一种假定的星形胶质细胞衍生的神经血管耦合剂,收缩而不是扩张实质小动脉。
J Cereb Blood Flow Metab. 2013 Apr;33(4):479-82. doi: 10.1038/jcbfm.2013.9. Epub 2013 Feb 6.
9
A systematic review of cerebral hemodynamic responses to neural activation following stroke.一项针对卒中后神经激活引起的脑血流动力学反应的系统评价。
J Neurol. 2013 Nov;260(11):2715-21. doi: 10.1007/s00415-013-6836-z. Epub 2013 Jan 12.
10
The smallest stroke: occlusion of one penetrating vessel leads to infarction and a cognitive deficit.最小的中风:一支穿支血管闭塞导致梗死和认知障碍。
Nat Neurosci. 2013 Jan;16(1):55-63. doi: 10.1038/nn.3278. Epub 2012 Dec 16.

缺血性脑内的神经血管调节

Neurovascular regulation in the ischemic brain.

作者信息

Jackman Katherine, Iadecola Costantino

机构信息

Brain and Mind Research Institute, Weill Cornell Medical College , New York, New York.

出版信息

Antioxid Redox Signal. 2015 Jan 10;22(2):149-60. doi: 10.1089/ars.2013.5669.

DOI:10.1089/ars.2013.5669
PMID:24328757
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4281847/
Abstract

SIGNIFICANCE

The brain has high energetic requirements and is therefore highly dependent on adequate cerebral blood supply. To compensate for dangerous fluctuations in cerebral perfusion, the circulation of the brain has evolved intrinsic safeguarding measures.

RECENT ADVANCES AND CRITICAL ISSUES

The vascular network of the brain incorporates a high degree of redundancy, allowing the redirection and redistribution of blood flow in the event of vascular occlusion. Furthermore, active responses such as cerebral autoregulation, which acts to maintain constant cerebral blood flow in response to changing blood pressure, and functional hyperemia, which couples blood supply with synaptic activity, allow the brain to maintain adequate cerebral perfusion in the face of varying supply or demand. In the presence of stroke risk factors, such as hypertension and diabetes, these protective processes are impaired and the susceptibility of the brain to ischemic injury is increased. One potential mechanism for the increased injury is that collateral flow arising from the normally perfused brain and supplying blood flow to the ischemic region is suppressed, resulting in more severe ischemia.

FUTURE DIRECTIONS

Approaches to support collateral flow may ameliorate the outcome of focal cerebral ischemia by rescuing cerebral perfusion in potentially viable regions of the ischemic territory.

摘要

意义

大脑对能量需求很高,因此高度依赖充足的脑供血。为了补偿脑灌注的危险波动,脑循环进化出了内在的保护机制。

最新进展与关键问题

脑的血管网络具有高度冗余性,在血管闭塞时允许血流重新定向和重新分配。此外,诸如脑自动调节(其作用是在血压变化时维持恒定的脑血流量)和功能性充血(将血液供应与突触活动相耦合)等主动反应,使大脑能够在供应或需求变化的情况下维持充足的脑灌注。在存在高血压和糖尿病等中风危险因素的情况下,这些保护过程会受到损害,大脑对缺血性损伤的易感性会增加。损伤增加的一个潜在机制是,由正常灌注的脑产生并向缺血区域供血的侧支血流受到抑制,导致更严重的缺血。

未来方向

支持侧支血流的方法可能通过挽救缺血区域潜在存活区域的脑灌注来改善局灶性脑缺血的结果。