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

• Published in: Nature communications Vol. 13; no. 1; p. 1382
• Main Authors: Fossey, Mary P. M., Balthazaar, Shane J. T., Squair, Jordan W., Williams, Alexandra M., Poormasjedi-Meibod, Malihe-Sadat, Nightingale, Tom E., Erskine, Erin, Hayes, Brian, Ahmadian, Mehdi, Jackson, Garett S., Hunter, Diana V., Currie, Katharine D., Tsang, Teresa S. M., Walter, Matthias, Little, Jonathan P., Ramer, Matt S., Krassioukov, Andrei V., West, Christopher R.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 16.03.2022; Nature Publishing Group; Nature Portfolio
• Subjects: 13; 14; 38; 59; 631/378/1687/1825; 631/443/376; 64/86; 692/4019/592; Animal models; Animals; Cardiac function; Cardiovascular diseases; Circuits; Heart; Heart diseases; Humanities and Social Sciences; Injury prevention; multidisciplinary; Muscle contraction; Prospective Studies; Rats; Science; Science (multidisciplinary); Spinal Cord; Spinal cord injuries; Spinal Cord Injuries - complications; Structure-function relationships; Sympathetic Nervous System; Ventricle; Ventricular Function, Left
• ISSN: 2041-1723; 2041-1723
• DOI: 10.1038/s41467-022-29066-1

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. By combining experimental models with prospective clinical studies, the authors show that spinal cord injury causes a rapid reduction in cardiac function that precedes structural changes, and that the loss of descending sympathetic control is the major cause of reduced cardiac function following spinal cord injury.