Mechanical Engineering, University College London, London, UK.
Centre for Advanced Biomedical Engineering, University College London, London, UK.
Sci Rep. 2018 Jan 22;8(1):1373. doi: 10.1038/s41598-017-19086-z.
The neurovascular mechanisms underpinning the local regulation of cerebral blood flow (CBF) and oxygen transport remain elusive. In this study we have combined novel in vivo imaging of cortical microvascular and mural cell architecture with mathematical modelling of blood flow and oxygen transport, to provide new insights into CBF regulation that would be inaccessible in a conventional experimental context. Our study indicates that vasoconstriction of smooth muscle actin-covered vessels, rather than pericyte-covered capillaries, induces stable reductions in downstream intravascular capillary and tissue oxygenation. We also propose that seemingly paradoxical observations in the literature around reduced blood velocity in response to arteriolar constrictions might be caused by a propagation of constrictions to upstream penetrating arterioles. We provide support for pericytes acting as signalling conduits for upstream smooth muscle activation, and erythrocyte deformation as a complementary regulatory mechanism. Finally, we caution against the use of blood velocity as a proxy measurement for flow. Our combined imaging-modelling platform complements conventional experimentation allowing cerebrovascular physiology to be probed in unprecedented detail.
神经血管机制是脑血流（CBF）和氧气运输局部调节的基础，但目前仍不清楚其具体机制。在这项研究中，我们将皮质微血管和壁细胞结构的新型活体成像与血流和氧气运输的数学模型相结合，为 CBF 调节提供了新的见解，这在传统的实验环境中是无法获得的。我们的研究表明，平滑肌肌动蛋白覆盖的血管而非周细胞覆盖的毛细血管收缩会导致下游血管内毛细血管和组织氧合的稳定减少。我们还提出，文献中关于血管收缩引起的血流速度降低的看似矛盾的观察结果可能是由于收缩向上游穿透小动脉传播所致。我们为周细胞作为上游平滑肌激活的信号传导途径提供了支持，并且红细胞变形作为一种补充调节机制。最后，我们提醒注意不要将血流速度用作流量的替代测量值。我们的联合成像-建模平台补充了传统实验，可以以前所未有的细节探测脑血管生理学。
