Arterial impulse model for the BOLD response to brief neural activation.
Arterial impulse model for the BOLD response to brief neural activation.
复制标题
对短暂神经激活的大胆反应的动脉冲动模型。
DOI：
10.1016/j.neuroimage.2015.08.068
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发表时间：
2016-01-01
期刊：
影响因子：
5.7
通讯作者：
Ress D
中科院分区：
文献类型：
--
作者：
Kim JH;Ress D
短暂的神经刺激所诱发的血氧水平依赖性（BOLD）信号，即血流动力学反应函数（HRF），是神经血管耦合的一个重要特征。HRF与脑血流量（CBF）和氧需求（脑氧代谢率（CMRO 2））提供的氧的局部瞬时变化直接相关。以前的努力来解释HRF依赖于假设，CBF产生的皮质实质内的非线性静脉扩张。相反，观察到的动力学对应于没有静脉容量变化的迅速动脉扩张。这项工作开发了一种替代的生物力学模型的BOLD响应的基础上的假设，即提示上游扩张创建一个动脉血流脉冲服从线性描述。这个流动模型耦合到一个连续描述的氧气输送。使用高分辨率fMRI的测量证明了该模型的有效性。该模型预测了氧饱和度沿毛细血管和静脉长度沿着的实质性空间变化，并通过相应的CBF和CMRO2响应的组合效应拟合了测量的HRF的变化范围。三个有趣的血液动力学参数之间的关系进行了预测。首先，在CBF和CMRO2响应之间存在具有近似单位斜率的偏移线性相关。第二，HRF下冲与相应的CBF下冲强烈相关。第三，晚期CMRO2反应可能有助于缓慢恢复到基线，延长HRF下冲。该模型提供了一个强大的数学框架来理解形成BOLD HRF的神经血管和神经代谢反应的动力学。
The blood oxygen level dependent (BOLD) signal evoked by brief neural stimulation, the hemodynamic response function (HRF), is a critical feature of neurovascular coupling. The HRF is directly related to local transient changes in oxygen supplied by cerebral blood flow (CBF) and oxygen demand, the cerebral metabolic rate of oxygen (CMRO2). Previous efforts to explain the HRF have relied upon the hypothesis that CBF produces a non-linear venous dilation within the cortical parenchyma. Instead, the observed dynamics correspond to prompt arterial dilation without venous volume change. This work develops an alternative biomechanical model for the BOLD response based on the hypothesis that prompt upstream dilation creates an arterial flow impulse amenable to linear description. This flow model is coupled to a continuum description of oxygen transport. Measurements using high-resolution fMRI demonstrate the efficacy of the model. The model predicts substantial spatial variations of the oxygen saturation along the length of capillaries and veins, and fits the varied gamut of measured HRFs by the combined effects of corresponding CBF and CMRO2 responses. Three interesting relationships among the hemodynamic parameters are predicted. First, there is an offset linear correlation with approximately unity slope between CBF and CMRO2 responses. Second, the HRF undershoot is strongly correlated to the corresponding CBF undershoot. Third, late-time-CMRO2 response can contribute to a slow recovery to baseline, lengthening the HRF undershoot. The model provides a powerful mathematical framework to understand the dynamics of neurovascular and neurometabolic responses that form the BOLD HRF.