Relative contributions of sympathetic, cholinergic, and myogenic mechanisms to cerebral autoregulation.

Relative contributions of sympathetic, cholinergic, and myogenic mechanisms to cerebral autoregulation.
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DOI:
10.1161/strokeaha.114.005293
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发表时间:
2014-06
期刊:
影响因子:
8.3
通讯作者:
Tan CO
Tan CO
中科院分区:
医学1区
文献类型:
--
作者:
Hamner JW;Tan CO

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先前的工作,旨在提高我们对人类大脑自动调节的理解,探讨了单独的生理机制的自动调节,但没有人试图巩固这些机制的个人角色到一个全面的模型的整体脑压力-流量关系。我们在43名健康志愿者中回顾性分析了α-肾上腺素能、毒蕈碱和钙通道介导机制药物阻断前后的这种关系,以确定交感神经、胆碱能和肌源性控制器对脑自动调节的相对贡献。采用投影寻踪回归分析评价药物阻断对脑压力-血流关系的影响。随后,使用协方差分解分析来确定这三种机制对脑自动调节的累积效应,以及它们是否可以完全解释它。交感神经、胆碱能和肌源性机制共占脑压力-流量关系的62%(p < 0.05),三种效应器中的每一种都有显著和不同的贡献。ANCOVA分解表明,肌源性效应器是大脑压力-流量关系的最大决定因素,但它们的作用在神经源性控制似乎占优势的自动调节区域之外。我们的研究结果表明,肌源性的影响发生在自动调节的活动区域之外,而神经源性的影响在很大程度上负责脑血流控制,然而,我们的脑自动调节模型留下了38%的脑压力-流量关系无法解释,这表明还有其他生理机制,有助于脑自动调节。
Prior work aimed at improving our understanding of human cerebral autoregulation has explored individual physiologic mechanisms of autoregulation in isolation, but none has attempted to consolidate the individual roles of these mechanisms into a comprehensive model of the overall cerebral pressure–flow relation. We retrospectively analyzed this relation before and after pharmacologic blockade of alpha-adrenergic, muscarinic, and calcium channel-mediated mechanisms in 43 healthy volunteers to determine the relative contributions of the sympathetic, cholinergic, and myogenic controllers to cerebral autoregulation. Projection pursuit regression was used to assess the effect of pharmacologic blockade on the cerebral pressure–flow relation. Subsequently, analysis of covariance decomposition was used to determine the cumulative effect of these three mechanisms on cerebral autoregulation and whether they can fully explain it. Sympathetic, cholinergic, and myogenic mechanisms together accounted for 62% of the cerebral pressure–flow relation (p < 0.05), with significant and distinct contributions from each of the three effectors. ANCOVA decomposition demonstrated that myogenic effectors were the largest determinant of the cerebral pressure–flow relation but their effect was outside of the autoregulatory region where neurogenic control appeared prepotent. Our results suggest that myogenic effects occur outside the active region of autoregulation, whereas neurogenic influences are largely responsible for cerebral blood flow control within it. However, our model of cerebral autoregulation left 38% of the cerebral pressure–flow relation unexplained, suggesting that there are other physiologic mechanisms that contribute to cerebral autoregulation.