Spinal cord injury impairs cardiac function due to impaired bulbospinal sympathetic control

Mary P.M. Fossey, Shane J.T. Balthazaar, Jordan W. Squair, Alexandra M. Williams, Malihe-Sadat Poormasjedi-Meibod, Tom E. Nightingale, Erin Erskine, Brian Hayes, Mehdi Ahmadian, Garett S Jackson, Dianna V Hunter, Katharine D Currie, Teresa Tsang, Matthias Walter, Jonathan P Little, Matt S Ramer, Andrei Krassioukov, Christopher West

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Spinal cord injury chronically alters cardiac structure and function and is associated with increased odds for cardiovascular disease. Here, we investigate the cardiac consequences of spinal cord injury on the acute-to-chronic continuum, and the contribution of altered bulbospinal sympathetic control to the decline in cardiac function following spinal cord injury. By combining experimental rat models of spinal cord injury with prospective clinical studies, we demonstrate that spinal cord injury causes a rapid and sustained reduction in left ventricular contractile function that precedes structural changes. In rodents, we experimentally demonstrate that this decline in left ventricular contractile function following spinal cord injury is underpinned by interrupted bulbospinal sympathetic control. In humans, we find that activation of the sympathetic circuitry below the level of spinal cord injury causes an immediate increase in systolic function. Our findings highlight the importance for early interventions to mitigate the cardiac functional decline following spinal cord injury.
Original languageEnglish
Article number1382
Number of pages16
JournalNature Communications
Issue number1
Early online date16 Mar 2022
Publication statusE-pub ahead of print - 16 Mar 2022


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