呼吸大小和频率的正常变异性导致呼气末PCO2（PETCO2）的呼吸到呼吸变异性，测量的变量，和二氧化碳的动脉分压（PaCO2），影响脑血流量（CBF）的独立变量。这项研究检查了PaCO2变异性对静息状态功能MRI（rs-fMRI）连通性模式的影响。感兴趣区域(ROI)-ROI和种子-体素一级双变量相关性，在两种静息状态条件下进行了测量rs-fMRI连通性的血液动力学反应功能（hrf）加权分析：（a）与PaCO2（poikilocapnia）呼吸到呼吸变化相关的正常呼吸，和(b)使用顺序再呼吸抑制PETCO2的呼吸-呼吸变异性的正常呼吸(等心痛)。潮气末PCO2（PETCO2）用作PaCO2波动的可测量替代品。在poikilocapnia期间,在小脑与额下和上背回（SG）之间发现了增强的功能连接，视觉皮层和枕骨梭状回；以及初级视觉网络（PVN）和海马结构之间。在等渗氮期间，这些关联没有被看到，在壳核和腔内皮质之间的皮质纹状体通路中发现了相当增强的功能连接，上颌皮质（SCC），和前皮质.我们得出的结论是，血管对PETCO2变化的反应至少解释了一些观察到的血液氧合水平依赖性（BOLD）信号的静息状态同步。
The normal variability in breath size and frequency results in breath-to-breath variability of end-tidal PCO2 (PETCO2), the measured variable, and arterial partial pressure of carbon dioxide (PaCO2), the independent variable affecting cerebral blood flow (CBF). This study examines the effect of variability in PaCO2 on the pattern of resting-state functional MRI (rs-fMRI) connectivity. A region of interest (ROI)-to-ROI and Seed-to-Voxel first-level bivariate correlation, hemodynamic response function (hrf)-weighted analysis for measuring rs-fMRI connectivity was performed during two resting-state conditions: (a) normal breathing associated with breath-to-breath variation in PaCO2 (poikilocapnia), and (b) normal breathing with breath-to-breath variability of PETCO2 dampened using sequential rebreathing (isocapnia). End-tidal PCO2 (PETCO2) was used as a measurable surrogate for fluctuations of PaCO2. During poikilocapnia, enhanced functional connections were found between the cerebellum and inferior frontal and supramarginal gyrus (SG), visual cortex and occipital fusiform gyrus; and between the primary visual network (PVN) and the hippocampal formation. During isocapnia, these associations were not seen, rather enhanced functional connections were identified in the corticostriatal pathway between the putamen and intracalacarine cortex, supracalcarine cortex (SCC), and precuneus cortex. We conclude that vascular responses to variations in PETCO2, account for at least some of the observed resting state synchronization of blood oxygenation level-dependent (BOLD) signals.
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