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

Author

Listed:
  • Mary P. M. Fossey

    (University of British Columbia
    University of British Columbia)

  • Shane J. T. Balthazaar

    (University of British Columbia
    University of British Columbia)

  • Jordan W. Squair

    (University of British Columbia)

  • Alexandra M. Williams

    (University of British Columbia
    University of British Columbia)

  • Malihe-Sadat Poormasjedi-Meibod

    (University of British Columbia)

  • Tom E. Nightingale

    (University of British Columbia
    University of Birmingham
    University of Birmingham, Edgabaston)

  • Erin Erskine

    (University of British Columbia
    University of British Columbia)

  • Brian Hayes

    (University of British Columbia)

  • Mehdi Ahmadian

    (University of British Columbia
    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
    University of Basel)

  • Jonathan P. Little

    (University of British Columbia)

  • Matt S. Ramer

    (University of British Columbia
    University of British Columbia)

  • Andrei V. Krassioukov

    (University of British Columbia
    University of British Columbia
    University of British Columbia
    Vancouver Coastal Health)

  • Christopher R. West

    (University of British Columbia
    University of British Columbia)

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.

Suggested Citation

  • 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. J, 2022. "Spinal cord injury impairs cardiac function due to impaired bulbospinal sympathetic control," Nature Communications, Nature, vol. 13(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-29066-1
    DOI: 10.1038/s41467-022-29066-1
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    References listed on IDEAS

    as
    1. Alexandra M. Williams & Neda Manouchehri & Erin Erskine & Keerit Tauh & Kitty So & Katelyn Shortt & Megan Webster & Shera Fisk & Avril Billingsley & Alex Munro & Seth Tigchelaar & Femke Streijger & Ky, 2020. "Cardio-centric hemodynamic management improves spinal cord oxygenation and mitigates hemorrhage in acute spinal cord injury," Nature Communications, Nature, vol. 11(1), pages 1-12, December.
    2. 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 & Giuse, 2021. "Neuroprosthetic baroreflex controls haemodynamics after spinal cord injury," Nature, Nature, vol. 590(7845), pages 308-314, February.
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