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Variability in integration of mechanisms associated with high tolerance to progressive reductions in central blood volume: the compensatory reserve

High tolerance to progressive reductions in central blood volume has been associated with higher heart rate (HR), peripheral vascular resistance (PVR), sympathetic nerve activity (SNA), and vagally mediated cardiac baroreflex sensitivity (BRS). Using a database of 116 subjects classified as high tol...

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Detalles Bibliográficos
Autores principales: Carter, Robert, Hinojosa‐Laborde, Carmen, Convertino, Victor A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4759043/
https://www.ncbi.nlm.nih.gov/pubmed/26884477
http://dx.doi.org/10.14814/phy2.12705
Descripción
Sumario:High tolerance to progressive reductions in central blood volume has been associated with higher heart rate (HR), peripheral vascular resistance (PVR), sympathetic nerve activity (SNA), and vagally mediated cardiac baroreflex sensitivity (BRS). Using a database of 116 subjects classified as high tolerance to presyncopal‐limited lower body negative pressure (LBNP), we tested the hypothesis that subjects with greater cardiac baroreflex withdrawal (i.e., BRS > 1.0) would demonstrate greater LBNP tolerance associated with higher HR, PVR, and SNA. Subjects underwent LBNP to presyncope. Mean and diastolic arterial pressure (MAP; DAP) was measured by finger photoplethysmography and BRS (down sequence) was autocalculated (WinCPRS) as ∆R‐R Interval/∆DAP. Down(BRS) (ms/mmHg) was used to dichotomize subjects into two groups (Group 1 = Down(BRS) > 1.0, N = 49, and Group 2 = Down(BRS) < 1.0, N = 67) at the time of presyncope. Muscle SNA was measured directly from the peroneal nerve via microneurography (N = 19) in subjects from Groups 1 (n = 9) and 2 (n = 10). Group 1 (Down(BRS) > 1.0) had lower HR (107 ± 19 vs. 131 ± 20 bpm), higher stroke volume (45 ± 15 vs. 36 ± 15 mL), less SNA (45 ± 13 vs. 53 ± 7 bursts/min), and less increase in PVR (4.1 ± 1.3 vs. 4.5 ± 2.6) compared to Group 2 (Down(BRS) < 1.0). Both groups had similar tolerance times (1849 ± 260 vs. 1839 ± 253 sec), MAP (78 ± 11 vs. 79 ± 12 mmHg), compensatory reserve index (CRI) (0.10 ± 0.03 vs. 0.09 ± 0.01), and cardiac output (4.5 ± 1.2 vs. 4.7 ± 1.1 L/min) at presyncope. Contrary to our hypothesis, higher HR, PVR, SNA, and BRS were not associated with greater tolerance to reduced central blood volume. These data are the first to demonstrate the variability and uniqueness of individual human physiological strategies designed to compensate for progressive reductions in central blood volume. The sum total of these integrated strategies is accurately reflected by the measurement of the compensatory reserve.