| Literature DB >> 33505019 |
Matthieu Gautier1,2, Lois Mahe1,2, Jan Elaine Soriano3,4,5,6, Andreas Rowald1,2, Jordan W Squair1,7,8,2,3,4,5,9,10,6, Arnaud Bichat1,2, Newton Cho1,2,11, Mark A Anderson1,2, Nicholas D James1,2, Jerome Gandar1,2, Anthony V Incognito6,12, Giuseppe Schiavone13, Zoe K Sarafis1,2, Achilleas Laskaratos1,2, Kay Bartholdi1,2, Robin Demesmaeker1,2, Salif Komi1,2, Charlotte Moerman8,2, Bita Vaseghi3,4,5, Berkeley Scott3,4,5,6, Ryan Rosentreter3,4,5,6, Claudia Kathe1,2, Jimmy Ravier1,2, Laura McCracken1,2, Xiaoyang Kang13, Nicolas Vachicouras13, Florian Fallegger13, Ileana Jelescu14, YunLong Cheng15, Qin Li15, Rik Buschman16, Nicolas Buse16, Tim Denison17,18, Sean Dukelow3,4,5,6,19, Rebecca Charbonneau4,6, Ian Rigby20, Steven K Boyd19, Philip J Millar12, Eduardo Martin Moraud8,2, Marco Capogrosso21, Fabien B Wagner1,2,22, Quentin Barraud1,2, Erwan Bezard15,22,23, Stéphanie P Lacour13, Jocelyne Bloch1,7,8,2, Grégoire Courtine24,25,26,27, Aaron A Phillips28,29,30,31,32.
Abstract
Spinal cord injury (SCI) induces haemodynamic instability that threatens survival1-3, 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.Entities:
Mesh：
Year: 2021 PMID： 33505019 DOI： 10.1038/s41586-020-03180-w
Source DB: PubMed Journal: Nature ISSN： 0028-0836 Impact factor: 49.962