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  • 1
    UID:
    (DE-627)1698861710
    Format: 8
    ISSN: 1878-5883
    Content: Patients with high cervical complete spinal cord injuries (tetraplegia) sustain damage to the autonomic neural pathways that influence cardiovascular functioning and produce variability in the heart rate (HR) and blood pressure (BP). In non-injured individuals, an inverse relationship exists between resting autonomic control of the heart (as evidenced by HR variability (HRV)) and BP variability (BPV). This study examined the relationship between HRV, BP and BPV in individuals with tetraplegic (n=10) and paraplegic (n=10) spinal cord injuries, and a group of healthy controls (n=14). Resting HRV at baseline and 24-hour ambulatory BP measurements were collected from electrocardiogram measures of each participant. HRV was quantified using time- and frequency-domain measures. The standard deviation of the BP measurements was used as an index of BPV. Multivariate analyses of variance were performed to examine group differences for laboratory-based and 24-h dependent variables. The MANOVAs for HRV parameters (λ(14,50)=.352, p=.010, η2=.407) and for BP indices and HR (λ(16,48)=.318, p=.013, η2=.436) were significant. Furthermore, in line with existing evidence, we found that vagally mediated HRV was inversely related to BPV in healthy controls. However, this relationship did not hold for the tetraplegia group (ρ〈|.42|), and mixed results were found for the paraplegia group (e.g., ρ〈|.29| for time domain HRV, ρ〉|.65| for low-frequency power). These results support the conclusion that the damage to the spinal sympathetic pathways to the heart found in people with tetraplegia causes a significant disruption in baroreflex control of BP.
    Note: Available online 10 December 2015 , Gesehen am 27.05.2020
    In: Journal of the neurological sciences, Amsterdam [u.a.] : Elsevier Science, 1964, 361(2016), Seite 52-59, 1878-5883
    In: volume:361
    In: year:2016
    In: pages:52-59
    In: extent:8
    Language: English
    URL: Volltext  (lizenzpflichtig)
    URL: Volltext  (lizenzpflichtig)
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