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, Diana V. Hunter, Katharine D. Currie, Teresa S. M. Tsang, Matthias Walter, Jonathan P. Little, Matt S. Ramer, Andrei V. Krassioukov () and Christopher R. West ()
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Mary P. M. Fossey: University of British Columbia
Shane J. T. Balthazaar: University of British Columbia
Jordan W. Squair: University of British Columbia
Alexandra M. Williams: University of British Columbia
Malihe-Sadat Poormasjedi-Meibod: University of British Columbia
Tom E. Nightingale: University of British Columbia
Erin Erskine: University of British Columbia
Brian Hayes: University of British Columbia
Mehdi Ahmadian: University of British Columbia
Garett S. Jackson: University of British Columbia
Diana V. Hunter: University of British Columbia
Katharine D. Currie: University of British Columbia
Teresa S. M. Tsang: University of British Columbia, Vancouver General and University of British Columbia Hospital Echocardiography Department
Matthias Walter: University of British Columbia
Jonathan P. Little: University of British Columbia
Matt S. Ramer: University of British Columbia
Andrei V. Krassioukov: University of British Columbia
Christopher R. West: University of British Columbia

Nature Communications, 2022, vol. 13, issue 1, 1-16

Abstract: Abstract 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.

Date: 2022
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-29066-1

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DOI: 10.1038/s41467-022-29066-1

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