High-speed vascular dynamics of the hemodynamic response.

High-speed vascular dynamics of the hemodynamic response.
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DOI:
10.1016/j.neuroimage.2010.09.036
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发表时间:
2011-01-15
期刊:
影响因子:
5.7
通讯作者:
Hillman EM
Hillman EM
中科院分区:
医学1区
文献类型:
--
作者:
Chen BR;Bouchard MB;McCaslin AF;Burgess SA;Hillman EM

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虽然已经提出了一系列细胞机制来控制神经血管耦合,但尚未确定一个全面的、协调的模型。为了适应这样的模型,候选机制必须表现出与“血流动力学响应”的血管表现一致的反应时间、空间范围和传播速度。因此,了解这些血管动力学是开发稳健的神经血管耦合模型的关键一步。在本研究中,我们利用暴露的啮齿动物体感皮层的高速光学成像来探索和表征功能性充血期间表面血管的时空动态。我们的高速、高分辨率光学成像方法使我们能够独立研究单个血管和实质离散区域的血流动力学响应,具有足够的分辨率来精确表征响应的微妙空间和时间特征。具体来说,我们探索响应刺激而发生第一次血流动力学变化的时间和地点,这些变化在小动脉和实质区域中传播的方向和速度,以及每个室返回其原始基线状态的相对时间。从这些结果中,我们可以得出结论,血流动力学反应是在实质中启动的,然后迅速扩散到表面小动脉。在最初发作后,我们发现证据表明反应通过目标小动脉的扩张在空间上向外传播。这种血管舒张的传播与每个小动脉内的血流方向无关。我们还发现了衰减阶段的证据,该阶段以更均匀的空间依赖性起作用,而不是沿着目标血管起作用,导致响应区域的外围首先返回到基线。我们假设不同的潜在细胞机制/信号通路导致响应启动和响应衰减。我们的结果促进了对血流动力学反应的基本理解,以及我们评估其参与神经血管耦合的潜在细胞机制的能力。
While a range of cellular mechanisms have been proposed to underlie control of neurovascular coupling, a comprehensive, reconciliatory model has yet to be determined. To fit with such a model, it is essential that candidate mechanisms exhibit reaction times, spatial ranges and speeds of propagation that are consistent with the vascular manifestations of the ‘hemodynamic response’. Understanding these vascular dynamics is therefore a critical step towards developing a robust model of neurovascular coupling. In this study, we utilize highspeed optical imaging of exposed rodent somatosensory cortex to explore and characterize the spatiotemporal dynamics of surface vessels during functional hyperemia. Our high-speed, high resolution optical imaging approach allows us to study the hemodynamic response independently in individual vessels, and in discrete regions of the parenchyma with enough resolution to precisely characterize subtle spatial and temporal features of the response. Specifically, we explore when and where the first hemodynamic changes occur in response to stimuli, the direction and speed at which these changes propagate in arterioles and regions of the parenchyma, and the relative timing at which each of these compartments returns to its original baseline state. From these results, we are able to conclude that the hemodynamic response is initiated in the parenchyma and then spreads rapidly to surface arterioles. Following the initial onset we find evidence that the response spreads spatially outwards via the dilation of targeted arterioles. This propagation of vasodilation is independent of the direction of blood flow within each arteriole. We also find evidence of a decay phase that acts with a more uniform spatial dependence, rather than along targeted vessels, causing the periphery of the responding region to return to baseline first. We hypothesize that different underlying cellular mechanisms/signaling pathways are responsible for the response initiation and the response decay. Our results advance a fundamental understanding of the hemodynamic response, as well as our ability to evaluate potential cellular mechanisms for their involvement in neurovascular coupling.
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期刊: The Journal of neuroscience : the official journal of the Society for Neuroscience
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