小柯机器人

加拿大卡尔加里大学Aaron A. Phillips、瑞士洛桑联邦理工学院Grégoire Courtine等研究人员合作发现，人工神经压力反射可控制脊髓损伤后的血流动力学。相关论文于2021年1月27日在线发表在《自然》杂志上。

研究人员表示，脊髓损伤（SCI）可引起血液动力学不稳定，从而威胁生存，损害神经系统恢复，增加心血管疾病的风险，并降低生活质量。在这种情况下，血流动力学的不稳定性是由于对位于脊髓中交感神经回路的指令中断，这阻止了自然压力反射控制这些回路来调节周围血管阻力。脊髓的硬膜外电刺激（EES）已表明可以补偿损伤后运动回路的指令中断，并可在瘫痪后恢复行走。

研究人员利用这些概念来开发了EES方案，以期望恢复SCI后的血流动力学稳定性。研究人员建立了一个临床前模型，这能够剖析交感神经回路的拓扑和动力学，并了解EES如何使这些回路整合。研究人员将这些空间和时间特征纳入刺激方案中，进而设想出一种可在闭环下运行的临床级仿生血液动力学调节器。在急性和慢性SCI后，这种“神经营养不良压力反射”可长时间控制啮齿动物、非人类灵长类动物和人类的血流动力学。

因此，研究人员将进行临床试验，从而将神经假体压力感受反射转变为SCI患者常用的疗法。 

附：英文原文

Title: Neuroprosthetic baroreflex controls haemodynamics after spinal cord injury

Author: Jordan W. Squair, Matthieu Gautier, Lois Mahe, Jan Elaine Soriano, Andreas Rowald, Arnaud Bichat, Newton Cho, Mark A. Anderson, Nicholas D. James, Jerome Gandar, Anthony V. Incognito, Giuseppe Schiavone, Zoe K. Sarafis, Achilleas Laskaratos, Kay Bartholdi, Robin Demesmaeker, Salif Komi, Charlotte Moerman, Bita Vaseghi, Berkeley Scott, Ryan Rosentreter, Claudia Kathe, Jimmy Ravier, Laura McCracken, Xiaoyang Kang, Nicolas Vachicouras, Florian Fallegger, Ileana Jelescu, YunLong Cheng, Qin Li, Rik Buschman, Nicolas Buse, Tim Denison, Sean Dukelow, Rebecca Charbonneau, Ian Rigby, Steven K. Boyd, Philip J. Millar, Eduardo Martin Moraud, Marco Capogrosso, Fabien B. Wagner, Quentin Barraud, Erwan Bezard, Stphanie P. Lacour, Jocelyne Bloch, Grgoire Courtine, Aaron A. Phillips

Issue&Volume: 2021-01-27

Abstract: Spinal cord injury (SCI) induces haemodynamic instability that threatens survival1,2,3, impairs neurological recovery4,5, increases the risk of cardiovascular disease6,7, and reduces quality of life8,9. Haemodynamic instability in this context is due to the interruption of supraspinal efferent commands to sympathetic circuits located in the spinal cord10, which prevents the natural baroreflex from controlling these circuits to adjust peripheral vascular resistance. Epidural electrical stimulation (EES) of the spinal cord has been shown to compensate for interrupted supraspinal commands to motor circuits below the injury11, and restored walking after paralysis12. Here, we leveraged these concepts to develop EES protocols that restored haemodynamic stability after SCI. We established a preclinical model that enabled us to dissect the topology and dynamics of the sympathetic circuits, and to understand how EES can engage these circuits. We incorporated these spatial and temporal features into stimulation protocols to conceive a clinical-grade biomimetic haemodynamic regulator that operates in a closed loop. This ‘neuroprosthetic baroreflex’ controlled haemodynamics for extended periods of time in rodents, non-human primates and humans, after both acute and chronic SCI. We will now conduct clinical trials to turn the neuroprosthetic baroreflex into a commonly available therapy for people with SCI.

DOI: 10.1038/s41586-020-03180-w

Source: https://www.nature.com/articles/s41586-020-03180-w

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