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酸碱平衡调节与感知:脑血管张力代谢调节中的加速器和制动器。

Acid-base regulation and sensing: Accelerators and brakes in metabolic regulation of cerebrovascular tone.

机构信息

Department of Biomedicine, Aarhus University, Aarhus, Denmark.

出版信息

J Cereb Blood Flow Metab. 2018 Apr;38(4):588-602. doi: 10.1177/0271678X17733868. Epub 2017 Oct 6.

DOI:10.1177/0271678X17733868
PMID:28984162
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5888856/
Abstract

Metabolic regulation of cerebrovascular tone directs blood flow to areas of increased neuronal activity and during disease states partially compensates for insufficient perfusion by enhancing blood flow in collateral blood vessels. Acid-base disturbances frequently occur as result of enhanced metabolism or insufficient blood supply, but despite definitive evidence that acid-base disturbances alter arterial tone, effects of individual acid-base equivalents and the underlying signaling mechanisms are still being debated. H is an important intra- and extracellular messenger that modifies cerebrovascular tone. In addition, low extracellular [HCO] promotes cerebrovascular contraction through an endothelium-dependent mechanism. CO alters arterial tone development via changes in intra- and extracellular pH but it is still controversial whether CO also has direct vasomotor effects. Vasocontractile responses to low extracellular [HCO] and acute CO-induced decreases in intracellular pH can counteract H-mediated vasorelaxation during metabolic and respiratory acidosis, respectively, and may thereby reduce the risk of capillary damage and cerebral edema that could be consequences of unopposed vasodilation. In this review, the signaling mechanisms for acid-base equivalents in cerebral arteries and the mechanisms of intracellular pH control in the arterial wall are discussed in the context of metabolic regulation of cerebrovascular tone and local perfusion.

摘要

脑血管张力的代谢调节指导血流流向神经元活动增加的区域,并且在疾病状态下,通过增强侧支血管的血流来部分补偿灌注不足。酸碱平衡紊乱经常是由于代谢增强或血液供应不足引起的,但是尽管有明确的证据表明酸碱平衡紊乱会改变动脉张力,但个别酸碱平衡当量的作用和潜在的信号机制仍存在争议。H 是一种重要的细胞内和细胞外信使,可调节脑血管张力。此外,低细胞外[HCO₃⁻]通过内皮细胞依赖机制促进脑血管收缩。CO 通过改变细胞内和细胞外 pH 值来改变动脉张力的发展,但 CO 是否具有直接的血管收缩作用仍存在争议。低细胞外[HCO₃⁻]引起的血管收缩反应和急性 CO 引起的细胞内 pH 值降低可以分别抵消代谢性和呼吸性酸中毒期间 H 介导的血管舒张,从而降低毛细血管损伤和脑水肿的风险,这可能是血管舒张不受抑制的后果。在这篇综述中,讨论了脑动脉中酸碱平衡当量的信号机制以及动脉壁中细胞内 pH 值控制的机制,这些机制与脑血管张力和局部灌注的代谢调节有关。

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Extracellular acidosis and very low [Na ] inhibit NBCn1- and NHE1-mediated net acid extrusion from mouse vascular smooth muscle cells.细胞外酸中毒和极低的[Na⁺]浓度会抑制小鼠血管平滑肌细胞中由NBCn1和NHE1介导的净酸排出。
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