High-Thoracic Spinal Cord Injury Impairs Biventricular Function and Blunts Cardiopulmonary Interactions in a Rodent Model

Abstract

Relative to the well-characterized detrimental effects of high-level spinal cord injury (SCI) on left ventricular (LV) function in both experimental models and clinical populations, the impacts of SCI on right ventricular (RV) function and cardiopulmonary interactions (for both LV and RV) remain largely unexplored. To address these gaps, we investigated biventricular function and cardiopulmonary interactions in adult male Wistar rats subjected to high-thoracic (T3) contusion SCI. Two weeks post-injury, animals were mechanically ventilated and instrumented for simultaneous LV, RV, and arterial pressure recordings. We show that SCI significantly impairs LV systolic performance, including reductions in peak pressure, mean pressure, and the maximum rate of pressure rise during systole (dP/dt_max), while RV dysfunction is more selective, sparing dP/dt_max but lowering peak pressure. Diastolic function remained largely intact in the LV, but RV end-diastolic pressure was significantly altered. This biventricular impairment was accompanied by marked resting systemic hypotension and attenuated mechanical ventilation-driven pressure oscillations across all waveforms, revealing a collapse of cardiopulmonary interactions post-SCI. The convergence of biventricular dysfunction, attenuated cardiopulmonary interactions, and resting systemic hypotension indicates a multisite disruption in cardiovascular control following SCI, introducing the right heart function and cardiopulmonary interactions as underrecognized targets for clinical monitoring and interventions.