Key result
T3 spinal cord injury in rats reduces MAP by ~17 mmHg and impairs LV contractility.
Why the study?
Pre-clinical therapies targeting neuroplasticity to improve motor function after incomplete spinal cord injury have rarely been tested for autonomic and cardiovascular benefits, requiring a model with spared descending sympathetic pathways alongside robust cardiovascular impairment.
Comparison
T3 spinal cord injury with 300 kdyn of force vs naïve
Design
Pre-clinical animal study
Follow-up
Fourteen days post-SCI
Authors
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Provides a rat model of SCI-induced hypotension and reduced contractility; leaves open translation to human neurorehabilitation.
Effect estimate: decrease of 17 ± 3 mmHg in MAP and 0.7 ± 0.1 mmHg/µL in LV contractility
p-value: p=<0.001
A novel T3 spinal cord injury model in rats successfully induces significant cardiovascular impairment while preserving sufficient white matter, providing a useful preclinical model for testing neuroplasticity-targeted rehabilitation therapies.
Wainman et al. (2021) studied Spinal cord injury (n=26). T3 spinal cord injury vs. Naïve group was evaluated on Mean arterial pressure and left ventricular contractility (end-systolic elastance) (decrease of 17 ± 3 mmHg in MAP and 0.7 ± 0.1 mmHg/µL in LV contractility, p=<0.001). A T3 spinal cord injury model in rats produced significant decreases in mean arterial pressure (17 ± 3 mmHg, p<0.001) and left ventricular contractility (0.7 ± 0.1 mmHg/µL, p<0.001).
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