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Cardiovagal baroreflex gain relates to sensory loss after spinal cord injury
Adina E Draghici1, J Andrew Taylor1
1Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, MA, United States of America; Cardiovascular Research Laboratory, Spaulding Hospital Cambridge, Cambridge, MA, United States of America.
Abstract:
Spinal cord injury (SCI) leads to autonomic nervous system damage, resulting in loss of sympathetic control to the vasculature and the heart proportional to injury level. Given maintained cardiac parasympathetic control, we hypothesized that SCI demonstrates a compensatory, higher baroreflex gain compared to able-bodied that relates to injury level (neurological and/or sensory). We compared baroreflex gain (average and across 10-20, 20-30, and 30-40 mmHg input stimuli) derived from neck chamber technique in SCI (N = 29; neurological level C1-T10, sensory zone of partial preservation C4-S4/5; ≤2 yrs since injury) and able-bodied (N = 14). Average gain tended to be higher in able-bodied compared to SCI (p = 0.06), primarily due to higher gains at 10-20 and 20-30 mmHg (p = 0.03, p = 0.06). In SCI, although gain was not related to neurological level, average gain and gain at 10-20 mmHg was related to sensory zone of partial preservation and resting RR-interval (all p < 0.02). Multiple regression showed that both sensory level and RR-interval were strongly predictive of average baroreflex gain (r2 = 0.41, p < 0.01) and gain at 10-20 mmHg (r2 = 0.51, p < 0.01); gain decreased with higher sensory zone of partial preservation and lower resting RR-interval. Moreover, gain was significantly lower in those with high sensory level compared to both able-bodied (average gain and gain at 10-20 and 20-30 mmHg p < 0.01) and those with low level injury (all p < 0.05). In SCI, sensory zone of partial preservation is more predictive of gain than neurological level. This might reflect that those with high level sensory injuries may have the lowest likelihood of intact cardiac sympathetic innervation and therefore lesser cardiac vagal responsiveness due to vagal-sympathetic interactions.
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