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
中科院分区:
文献类型:
--
作者:
Hamner JW;Tan CO
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.