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1 Center for Biomedical Engineering, University of Kentucky, Lexington, Kentucky, United States
2 Center for Biomedical Engineering, University of Kentucky, Lexington, Kentucky, United States; Dept. of Physiology, University of Kentucky, United Kingdom
3 Electrical and Computer Engineering, University of Kentucky, Lexington, Kentucky, United States
4 Department of Physical Medicine and Rehabilitation, University of Kentucky, Lexington, Kentucky, United States
5 Cardinal Hill Rehap Hospital, United States
* To whom correspondence should be addressed. E-mail: jevans1{at}pop.uky.edu.
We investigated autonomic control of cardiovascular function in able-bodied (AB), paraplegic (PARA) and tetraplegic (TETRA) subjects in response to head up tilt (HUT) following spinal cord injury (SCI). We evaluated spectral power of blood pressure (BP), baroreflex sensitivity (BRS), baroreflex effectiveness index (BEI), occurrence of systolic blood pressure (SBP) ramps, baroreflex sequences and cross correlation of SBP with heart rate (HR) in low (0.04-0.15 Hz) and high (0.15-0.4 Hz) frequency regions. During tilt, AB and PARA effectively regulated BP and HR but TETRA did not. The numbers of SBP ramps and percentages of heartbeats involved in SBP ramps and baroreflex sequences increased in AB, were unchanged in PARA and declined in TETRA. BRS was lowest in PARA and declined with tilt in all groups. BEI was greatest in AB, and declined with tilt in all groups. Low frequency power of BP and the peak of the SBP/HR cross correlation magnitude were greatest in AB, increased during HUT in AB, remained unchanged in PARA, and declined in TETRA. The peak cross correlation magnitude in HF decreased with tilt in all groups. Our data indicate that SCI results in decreased stimulation of arterial baroreceptors and less engagement of feedback control as demonstrated by their lower: 1) spectral power of BP, 2) number (and percentages) of SBP ramps and barosequences 3) cross correlation magnitude of SBP/HR, 4) BEI and 5) changes in delay between SBP/HR. Diminished vasomotion and impaired baroreflex regulation may be major contributors to decreased orthostatic tolerance following injury.
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