Abstract
It is well recognized that the interruption in bulbospinal sympathetic projections is the main cause of cardiovascular instability in individuals and experimental animals with spinal cord injury (SCI). Whether interrupted bulbospinal sympathetic projections contribute to cardiac dysfunction directly (i.e. input to the heart) or indirectly (i.e. vascular influences that alter loading conditions on the heart) post-SCI remains unknown, as does the potential effect of SCI-induced alterations in parasympathetic control on heart function. We employed a sequential pharmacological blockade approach to bridge this knowledge gap and additionally examined whether acute intermittent hypoxia (AIH) is capable of neuromodulating the heart post-SCI. In two experiments, rats were given T3 contusion SCI and survived for 2 weeks. At 2 weeks post-SCI, rats were instrumented with left ventricular and arterial catheters to assess cardiovascular function in response to either a sequential pharmacological blockade targeting different sites of the autonomic neuraxis (experiment 1) or AIH (experiment 2). The findings from experiment 1 revealed that impaired direct sympathetic transmission to the heart underlies the majority of the SCI-induced reduction in heart function post-SCI. The findings from experiment 2 revealed that a single-session of AIH increased left ventricular pressure generation and arterial blood pressure immediately and up to 90 min post-AIH. Together, our findings demonstrate that disrupted bulbospinal sympathetic pathways contribute directly to the SCI-induced impairment in left ventricular function. We also show that a single session of AIH is capable of neuromodulating the heart post-SCI. KEY POINTS: The loss of sympathetic transmission to the heart is the main cause of reduced cardiac function in a rodent model of spinal cord injury (SCI). Parasympathetic control remains unaltered post-SCI and does not contribute to reduced cardiac function post-SCI. Acute intermittent hypoxia neuromodulates the heart and increases left ventricular pressure generating capacity.