Effect of head-down-tilt bed rest and hypovolemia on dynamic regulation of heart rate and blood pressure
Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, and Space Medicine Laboratory, Department of Internal Medicine, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235 Adaptation to head-down-tilt bed rest leads to an apparent abnormalit...
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Published in | American journal of physiology. Regulatory, integrative and comparative physiology Vol. 279; no. 6; pp. 2189 - R2199 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Legacy CDMS
01.12.2000
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Subjects | |
Online Access | Get full text |
ISSN | 0363-6119 1522-1490 |
DOI | 10.1152/ajpregu.2000.279.6.r2189 |
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Abstract | Institute for Exercise and Environmental Medicine, Presbyterian
Hospital of Dallas, and Space Medicine Laboratory, Department of
Internal Medicine, The University of Texas Southwestern Medical Center
at Dallas, Dallas, Texas 75235
Adaptation to head-down-tilt bed rest leads to an apparent
abnormality of baroreflex regulation of cardiac period. We hypothesized that this "deconditioning response" could primarily be a result of
hypovolemia, rather than a unique adaptation of the autonomic nervous
system to bed rest. To test this hypothesis, nine healthy subjects
underwent 2 wk of 6° head-down bed rest. One year later, five of
these same subjects underwent acute hypovolemia with furosemide to
produce the same reductions in plasma volume observed after bed rest.
We took advantage of power spectral and transfer function analysis to
examine the dynamic relationship between blood pressure (BP) and R-R
interval. We found that 1 ) there were no significant differences between these two interventions with respect to changes in
numerous cardiovascular indices, including cardiac filling pressures,
arterial pressure, cardiac output, or stroke volume; 2 )
normalized high-frequency (0.15-0.25 Hz) power of R-R interval variability decreased significantly after both conditions, consistent with similar degrees of vagal withdrawal; 3 ) transfer
function gain (BP to R-R interval), used as an index of
arterial-cardiac baroreflex sensitivity, decreased significantly to a
similar extent after both conditions in the high-frequency range; the
gain also decreased similarly when expressed as BP to heart rate × stroke volume, which provides an index of the ability of the
baroreflex to alter BP by modifying systemic flow; and 4 )
however, the low-frequency (0.05-0.15 Hz) power of systolic BP
variability decreased after bed rest ( 22%) compared with an increase
(+155%) after acute hypovolemia, suggesting a differential response
for the regulation of vascular resistance (interaction, P < 0.05). The similarity of changes in the reflex control of the
circulation under both conditions is consistent with the hypothesis
that reductions in plasma volume may be largely responsible for the
observed changes in cardiac baroreflex control after bed rest. However,
changes in vasomotor function associated with these two conditions may be different and may suggest a cardiovascular remodeling after bed rest.
plasma volume; baroreflex; spectral analysis; men; furosemide; microgravity |
---|---|
AbstractList | Adaptation to head-down-tilt bed rest leads to an apparent abnormality of baroreflex regulation of cardiac period. We hypothesized that this "deconditioning response" could primarily be a result of hypovolemia, rather than a unique adaptation of the autonomic nervous system to bed rest. To test this hypothesis, nine healthy subjects underwent 2 wk of -6 degrees head-down bed rest. One year later, five of these same subjects underwent acute hypovolemia with furosemide to produce the same reductions in plasma volume observed after bed rest. We took advantage of power spectral and transfer function analysis to examine the dynamic relationship between blood pressure (BP) and R-R interval. We found that 1) there were no significant differences between these two interventions with respect to changes in numerous cardiovascular indices, including cardiac filling pressures, arterial pressure, cardiac output, or stroke volume; 2) normalized high-frequency (0.15-0.25 Hz) power of R-R interval variability decreased significantly after both conditions, consistent with similar degrees of vagal withdrawal; 3) transfer function gain (BP to R-R interval), used as an index of arterial-cardiac baroreflex sensitivity, decreased significantly to a similar extent after both conditions in the high-frequency range; the gain also decreased similarly when expressed as BP to heart rate x stroke volume, which provides an index of the ability of the baroreflex to alter BP by modifying systemic flow; and 4) however, the low-frequency (0.05-0.15 Hz) power of systolic BP variability decreased after bed rest (-22%) compared with an increase (+155%) after acute hypovolemia, suggesting a differential response for the regulation of vascular resistance (interaction, P < 0.05). The similarity of changes in the reflex control of the circulation under both conditions is consistent with the hypothesis that reductions in plasma volume may be largely responsible for the observed changes in cardiac baroreflex control after bed rest. However, changes in vasomotor function associated with these two conditions may be different and may suggest a cardiovascular remodeling after bed rest. Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, and Space Medicine Laboratory, Department of Internal Medicine, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235 Adaptation to head-down-tilt bed rest leads to an apparent abnormality of baroreflex regulation of cardiac period. We hypothesized that this "deconditioning response" could primarily be a result of hypovolemia, rather than a unique adaptation of the autonomic nervous system to bed rest. To test this hypothesis, nine healthy subjects underwent 2 wk of 6° head-down bed rest. One year later, five of these same subjects underwent acute hypovolemia with furosemide to produce the same reductions in plasma volume observed after bed rest. We took advantage of power spectral and transfer function analysis to examine the dynamic relationship between blood pressure (BP) and R-R interval. We found that 1 ) there were no significant differences between these two interventions with respect to changes in numerous cardiovascular indices, including cardiac filling pressures, arterial pressure, cardiac output, or stroke volume; 2 ) normalized high-frequency (0.15-0.25 Hz) power of R-R interval variability decreased significantly after both conditions, consistent with similar degrees of vagal withdrawal; 3 ) transfer function gain (BP to R-R interval), used as an index of arterial-cardiac baroreflex sensitivity, decreased significantly to a similar extent after both conditions in the high-frequency range; the gain also decreased similarly when expressed as BP to heart rate × stroke volume, which provides an index of the ability of the baroreflex to alter BP by modifying systemic flow; and 4 ) however, the low-frequency (0.05-0.15 Hz) power of systolic BP variability decreased after bed rest ( 22%) compared with an increase (+155%) after acute hypovolemia, suggesting a differential response for the regulation of vascular resistance (interaction, P < 0.05). The similarity of changes in the reflex control of the circulation under both conditions is consistent with the hypothesis that reductions in plasma volume may be largely responsible for the observed changes in cardiac baroreflex control after bed rest. However, changes in vasomotor function associated with these two conditions may be different and may suggest a cardiovascular remodeling after bed rest. plasma volume; baroreflex; spectral analysis; men; furosemide; microgravity Adaptation to head-down-tilt bed rest leads to an apparent abnormality of baroreflex regulation of cardiac period. We hypothesized that this “deconditioning response” could primarily be a result of hypovolemia, rather than a unique adaptation of the autonomic nervous system to bed rest. To test this hypothesis, nine healthy subjects underwent 2 wk of −6° head-down bed rest. One year later, five of these same subjects underwent acute hypovolemia with furosemide to produce the same reductions in plasma volume observed after bed rest. We took advantage of power spectral and transfer function analysis to examine the dynamic relationship between blood pressure (BP) and R-R interval. We found that 1) there were no significant differences between these two interventions with respect to changes in numerous cardiovascular indices, including cardiac filling pressures, arterial pressure, cardiac output, or stroke volume; 2) normalized high-frequency (0.15–0.25 Hz) power of R-R interval variability decreased significantly after both conditions, consistent with similar degrees of vagal withdrawal; 3) transfer function gain (BP to R-R interval), used as an index of arterial-cardiac baroreflex sensitivity, decreased significantly to a similar extent after both conditions in the high-frequency range; the gain also decreased similarly when expressed as BP to heart rate × stroke volume, which provides an index of the ability of the baroreflex to alter BP by modifying systemic flow; and 4) however, the low-frequency (0.05–0.15 Hz) power of systolic BP variability decreased after bed rest (−22%) compared with an increase (+155%) after acute hypovolemia, suggesting a differential response for the regulation of vascular resistance (interaction, P < 0.05). The similarity of changes in the reflex control of the circulation under both conditions is consistent with the hypothesis that reductions in plasma volume may be largely responsible for the observed changes in cardiac baroreflex control after bed rest. However, changes in vasomotor function associated with these two conditions may be different and may suggest a cardiovascular remodeling after bed rest. Adaptation to head-down-tilt bed rest leads to an apparent abnormality of baroreflex regulation of cardiac period. We hypothesized that this "deconditioning response" could primarily be a result of hypovolemia, rather than a unique adaptation of the autonomic nervous system to bed rest. To test this hypothesis, nine healthy subjects underwent 2 wk of -6 degrees head-down bed rest. One year later, five of these same subjects underwent acute hypovolemia with furosemide to produce the same reductions in plasma volume observed after bed rest. We took advantage of power spectral and transfer function analysis to examine the dynamic relationship between blood pressure (BP) and R-R interval. We found that 1) there were no significant differences between these two interventions with respect to changes in numerous cardiovascular indices, including cardiac filling pressures, arterial pressure, cardiac output, or stroke volume; 2) normalized high-frequency (0.15-0.25 Hz) power of R-R interval variability decreased significantly after both conditions, consistent with similar degrees of vagal withdrawal; 3) transfer function gain (BP to R-R interval), used as an index of arterial-cardiac baroreflex sensitivity, decreased significantly to a similar extent after both conditions in the high-frequency range; the gain also decreased similarly when expressed as BP to heart rate x stroke volume, which provides an index of the ability of the baroreflex to alter BP by modifying systemic flow; and 4) however, the low-frequency (0.05-0.15 Hz) power of systolic BP variability decreased after bed rest (-22%) compared with an increase (+155%) after acute hypovolemia, suggesting a differential response for the regulation of vascular resistance (interaction, P < 0.05). The similarity of changes in the reflex control of the circulation under both conditions is consistent with the hypothesis that reductions in plasma volume may be largely responsible for the observed changes in cardiac baroreflex control after bed rest. However, changes in vasomotor function associated with these two conditions may be different and may suggest a cardiovascular remodeling after bed rest.Adaptation to head-down-tilt bed rest leads to an apparent abnormality of baroreflex regulation of cardiac period. We hypothesized that this "deconditioning response" could primarily be a result of hypovolemia, rather than a unique adaptation of the autonomic nervous system to bed rest. To test this hypothesis, nine healthy subjects underwent 2 wk of -6 degrees head-down bed rest. One year later, five of these same subjects underwent acute hypovolemia with furosemide to produce the same reductions in plasma volume observed after bed rest. We took advantage of power spectral and transfer function analysis to examine the dynamic relationship between blood pressure (BP) and R-R interval. We found that 1) there were no significant differences between these two interventions with respect to changes in numerous cardiovascular indices, including cardiac filling pressures, arterial pressure, cardiac output, or stroke volume; 2) normalized high-frequency (0.15-0.25 Hz) power of R-R interval variability decreased significantly after both conditions, consistent with similar degrees of vagal withdrawal; 3) transfer function gain (BP to R-R interval), used as an index of arterial-cardiac baroreflex sensitivity, decreased significantly to a similar extent after both conditions in the high-frequency range; the gain also decreased similarly when expressed as BP to heart rate x stroke volume, which provides an index of the ability of the baroreflex to alter BP by modifying systemic flow; and 4) however, the low-frequency (0.05-0.15 Hz) power of systolic BP variability decreased after bed rest (-22%) compared with an increase (+155%) after acute hypovolemia, suggesting a differential response for the regulation of vascular resistance (interaction, P < 0.05). The similarity of changes in the reflex control of the circulation under both conditions is consistent with the hypothesis that reductions in plasma volume may be largely responsible for the observed changes in cardiac baroreflex control after bed rest. However, changes in vasomotor function associated with these two conditions may be different and may suggest a cardiovascular remodeling after bed rest. |
Audience | PUBLIC |
Author | Zuckerman, Julie H Zhang, Rong Levine, Benjamin D Iwasaki, Ken-Ichi Pawelczyk, James A |
Author_xml | – sequence: 1 fullname: Iwasaki, Ken-Ichi – sequence: 2 fullname: Zhang, Rong – sequence: 3 fullname: Zuckerman, Julie H – sequence: 4 fullname: Pawelczyk, James A – sequence: 5 fullname: Levine, Benjamin D |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/11080085$$D View this record in MEDLINE/PubMed |
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Keywords | Human Support, U.s. Gov't, Non-P.h.s Nasa Discipline Cardiopulmonary Blood Pressure/drug Effects/physiology Hypovolemia Homeostasis/physiology Support, U.s. Gov't, P.h.s Cardiac Output Non-Nasa Center Male Head-Down Tilt/physiology Hemodynamic Processes/drug Effects/physiology Stroke Volume Heart Rate/drug Effects/physiology Furosemide/pharmacology Electrocardiography Adult Weightlessness Simulation Baroreflex/physiology NASA Discipline Cardiopulmonary Non-NASA Center |
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PublicationYear | 2000 |
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Snippet | Institute for Exercise and Environmental Medicine, Presbyterian
Hospital of Dallas, and Space Medicine Laboratory, Department of
Internal Medicine, The... Adaptation to head-down-tilt bed rest leads to an apparent abnormality of baroreflex regulation of cardiac period. We hypothesized that this "deconditioning... Adaptation to head-down-tilt bed rest leads to an apparent abnormality of baroreflex regulation of cardiac period. We hypothesized that this “deconditioning... |
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SubjectTerms | Adult Aerospace Medicine Baroreflex - physiology Blood Pressure - drug effects Blood Pressure - physiology Cardiac Output Electrocardiography Furosemide - pharmacology Head-Down Tilt - physiology Heart Rate - drug effects Heart Rate - physiology Hemodynamics - drug effects Hemodynamics - physiology Homeostasis - physiology Humans Hypovolemia Male Stroke Volume Weightlessness Simulation |
Title | Effect of head-down-tilt bed rest and hypovolemia on dynamic regulation of heart rate and blood pressure |
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