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正常大脑以及高血压、中风和阿尔茨海默病中的神经血管耦合。

Neurovascular coupling in the normal brain and in hypertension, stroke, and Alzheimer disease.

作者信息

Girouard Helene, Iadecola Costantino

机构信息

Division of Neurobiology, Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA.

出版信息

J Appl Physiol (1985). 2006 Jan;100(1):328-35. doi: 10.1152/japplphysiol.00966.2005.

DOI:10.1152/japplphysiol.00966.2005
PMID:16357086
Abstract

The brain is critically dependent on a continuous supply of blood to function. Therefore, the cerebral vasculature is endowed with neurovascular control mechanisms that assure that the blood supply of the brain is commensurate to the energy needs of its cellular constituents. The regulation of cerebral blood flow (CBF) during brain activity involves the coordinated interaction of neurons, glia, and vascular cells. Thus, whereas neurons and glia generate the signals initiating the vasodilation, endothelial cells, pericytes, and smooth muscle cells act in concert to transduce these signals into carefully orchestrated vascular changes that lead to CBF increases focused to the activated area and temporally linked to the period of activation. Neurovascular coupling is disrupted in pathological conditions, such as hypertension, Alzheimer disease, and ischemic stroke. Consequently, CBF is no longer matched to the metabolic requirements of the tissue. This cerebrovascular dysregulation is mediated in large part by the deleterious action of reactive oxygen species on cerebral blood vessels. A major source of cerebral vascular radicals in models of hypertension and Alzheimer disease is the enzyme NADPH oxidase. These findings, collectively, highlight the importance of neurovascular coupling to the health of the normal brain and suggest a therapeutic target for improving brain function in pathologies associated with cerebrovascular dysfunction.

摘要

大脑的正常运作严重依赖于持续的血液供应。因此,脑血管系统具备神经血管控制机制,以确保大脑的血液供应与其细胞成分的能量需求相匹配。大脑活动期间脑血流量(CBF)的调节涉及神经元、神经胶质细胞和血管细胞的协同相互作用。因此,虽然神经元和神经胶质细胞产生引发血管舒张的信号,但内皮细胞、周细胞和平滑肌细胞协同作用,将这些信号转化为精心编排的血管变化,从而导致CBF增加,集中于激活区域并在时间上与激活期相关联。在高血压、阿尔茨海默病和缺血性中风等病理状态下,神经血管耦合会受到破坏。因此,CBF不再与组织的代谢需求相匹配。这种脑血管调节异常在很大程度上是由活性氧对脑血管的有害作用介导的。在高血压和阿尔茨海默病模型中,脑血管自由基的一个主要来源是酶NADPH氧化酶。这些发现共同强调了神经血管耦合对正常大脑健康的重要性,并为改善与脑血管功能障碍相关疾病中的脑功能提供了一个治疗靶点。

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