Plasma volume restoration with salt tablets and water after bed rest prevents orthostatic hypotension and changes in supine hemodynamic and endocrine variables

1 Human Adaptation and Countermeasures Office, Wyle Laboratories, Inc.; 2 Division of Space Life Sciences, Universities Space Research Association; and 3 Astronaut Office and 4 Human Adaptation and Countermeasures Office, National Aeronautics and Space Administration Johnson Space Center, Houston, T...

Full description

Saved in:
Bibliographic Details
Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 288; no. 2; pp. H839 - H847
Main Authors Waters, Wendy W, Platts, Steven H, Mitchell, Brett M, Whitson, Peggy A, Meck, Janice V
Format Journal Article
LanguageEnglish
Published United States 01.02.2005
Subjects
Online AccessGet full text
ISSN0363-6135
1522-1539
DOI10.1152/ajpheart.00220.2004

Cover

Loading…
Abstract 1 Human Adaptation and Countermeasures Office, Wyle Laboratories, Inc.; 2 Division of Space Life Sciences, Universities Space Research Association; and 3 Astronaut Office and 4 Human Adaptation and Countermeasures Office, National Aeronautics and Space Administration Johnson Space Center, Houston, Texas Submitted 5 March 2004 ; accepted in final form 6 October 2004 Head-down bed rest changes the values of many cardiovascular and endocrine variables and also elicits significant hypovolemia. Because previous studies had not controlled for hypovolemia, it is unknown whether the reported changes were primary effects of bed rest or secondary effects of bed rest-induced hypovolemia. We hypothesized that restoring plasma volume with salt tablets and water after 12 days of head-down bed rest would result in an absence of hemodynamic and endocrine changes and a reduced incidence of orthostatic hypotension. In 10 men, we measured changes from pre-bed-rest to post-bed-rest in venous and arterial pressures; heart rate; stroke volume; cardiac output; vascular resistance; plasma norepinephrine, epinephrine, vasopressin, renin activity (PRA), and aldosterone responses to different tilt levels (0°, –10°, 20°, 30°, and 70°); and plasma volume and platelet 2 - and lymphocyte 2 -adrenoreceptor densities and affinities (0° tilt only). Fluid loading at the end of bed rest restored plasma volume and resulted in the absence of post-bed-rest orthostatic hypotension and changes in supine hemodynamic and endocrine variables. Fluid loading did not prevent post-bed-rest increases in 2 -adrenoreceptor density or decreases in the aldosterone-to-PRA ratio ( P = 0.05 for each). Heart rate, epinephrine, and PRA responses to upright tilt after bed rest were increased ( P < 0.05), despite the fluid load. These results suggest that incidents of orthostatic hypotension and many of the changes in supine hemodynamic and endocrine variables in volume-depleted bed-rested subjects occur secondarily to the hypovolemia. Despite normovolemia after bed rest, 2 -adrenoreceptors were upregulated, and heart rate, epinephrine, and PRA responses to tilt were augmented, indicating that these changes are independent of volume depletion. simulated microgravity; cardiovascular; hypovolemia; cardiopulmonary-arterial baroreceptor reflex interaction; adrenergic receptors
AbstractList Head-down bed rest changes the values of many cardiovascular and endocrine variables and also elicits significant hypovolemia. Because previous studies had not controlled for hypovolemia, it is unknown whether the reported changes were primary effects of bed rest or secondary effects of bed rest-induced hypovolemia. We hypothesized that restoring plasma volume with salt tablets and water after 12 days of head-down bed rest would result in an absence of hemodynamic and endocrine changes and a reduced incidence of orthostatic hypotension. In 10 men, we measured changes from pre-bed-rest to post-bed-rest in venous and arterial pressures; heart rate; stroke volume; cardiac output; vascular resistance; plasma norepinephrine, epinephrine, vasopressin, renin activity (PRA), and aldosterone responses to different tilt levels (0 degrees, -10 degrees, 20 degrees, 30 degrees, and 70 degrees); and plasma volume and platelet alpha2- and lymphocyte beta2-adrenoreceptor densities and affinities (0 degrees tilt only). Fluid loading at the end of bed rest restored plasma volume and resulted in the absence of post-bed-rest orthostatic hypotension and changes in supine hemodynamic and endocrine variables. Fluid loading did not prevent post-bed-rest increases in beta2-adrenoreceptor density or decreases in the aldosterone-to-PRA ratio (P = 0.05 for each). Heart rate, epinephrine, and PRA responses to upright tilt after bed rest were increased (P < 0.05), despite the fluid load. These results suggest that incidents of orthostatic hypotension and many of the changes in supine hemodynamic and endocrine variables in volume-depleted bed-rested subjects occur secondarily to the hypovolemia. Despite normovolemia after bed rest, beta2-adrenoreceptors were upregulated, and heart rate, epinephrine, and PRA responses to tilt were augmented, indicating that these changes are independent of volume depletion.
Head-down bed rest changes the values of many cardiovascular and endocrine variables and also elicits significant hypovolemia. Because previous studies had not controlled for hypovolemia, it is unknown whether the reported changes were primary effects of bed rest or secondary effects of bed rest-induced hypovolemia. We hypothesized that restoring plasma volume with salt tablets and water after 12 days of head-down bed rest would result in an absence of hemodynamic and endocrine changes and a reduced incidence of orthostatic hypotension. In 10 men, we measured changes from pre-bed-rest to post-bed-rest in venous and arterial pressures; heart rate; stroke volume; cardiac output; vascular resistance; plasma norepinephrine, epinephrine, vasopressin, renin activity (PRA), and aldosterone responses to different tilt levels (0 degrees, -10 degrees, 20 degrees, 30 degrees, and 70 degrees); and plasma volume and platelet alpha2- and lymphocyte beta2-adrenoreceptor densities and affinities (0 degrees tilt only). Fluid loading at the end of bed rest restored plasma volume and resulted in the absence of post-bed-rest orthostatic hypotension and changes in supine hemodynamic and endocrine variables. Fluid loading did not prevent post-bed-rest increases in beta2-adrenoreceptor density or decreases in the aldosterone-to-PRA ratio (P = 0.05 for each). Heart rate, epinephrine, and PRA responses to upright tilt after bed rest were increased (P < 0.05), despite the fluid load. These results suggest that incidents of orthostatic hypotension and many of the changes in supine hemodynamic and endocrine variables in volume-depleted bed-rested subjects occur secondarily to the hypovolemia. Despite normovolemia after bed rest, beta2-adrenoreceptors were upregulated, and heart rate, epinephrine, and PRA responses to tilt were augmented, indicating that these changes are independent of volume depletion.Head-down bed rest changes the values of many cardiovascular and endocrine variables and also elicits significant hypovolemia. Because previous studies had not controlled for hypovolemia, it is unknown whether the reported changes were primary effects of bed rest or secondary effects of bed rest-induced hypovolemia. We hypothesized that restoring plasma volume with salt tablets and water after 12 days of head-down bed rest would result in an absence of hemodynamic and endocrine changes and a reduced incidence of orthostatic hypotension. In 10 men, we measured changes from pre-bed-rest to post-bed-rest in venous and arterial pressures; heart rate; stroke volume; cardiac output; vascular resistance; plasma norepinephrine, epinephrine, vasopressin, renin activity (PRA), and aldosterone responses to different tilt levels (0 degrees, -10 degrees, 20 degrees, 30 degrees, and 70 degrees); and plasma volume and platelet alpha2- and lymphocyte beta2-adrenoreceptor densities and affinities (0 degrees tilt only). Fluid loading at the end of bed rest restored plasma volume and resulted in the absence of post-bed-rest orthostatic hypotension and changes in supine hemodynamic and endocrine variables. Fluid loading did not prevent post-bed-rest increases in beta2-adrenoreceptor density or decreases in the aldosterone-to-PRA ratio (P = 0.05 for each). Heart rate, epinephrine, and PRA responses to upright tilt after bed rest were increased (P < 0.05), despite the fluid load. These results suggest that incidents of orthostatic hypotension and many of the changes in supine hemodynamic and endocrine variables in volume-depleted bed-rested subjects occur secondarily to the hypovolemia. Despite normovolemia after bed rest, beta2-adrenoreceptors were upregulated, and heart rate, epinephrine, and PRA responses to tilt were augmented, indicating that these changes are independent of volume depletion.
1 Human Adaptation and Countermeasures Office, Wyle Laboratories, Inc.; 2 Division of Space Life Sciences, Universities Space Research Association; and 3 Astronaut Office and 4 Human Adaptation and Countermeasures Office, National Aeronautics and Space Administration Johnson Space Center, Houston, Texas Submitted 5 March 2004 ; accepted in final form 6 October 2004 Head-down bed rest changes the values of many cardiovascular and endocrine variables and also elicits significant hypovolemia. Because previous studies had not controlled for hypovolemia, it is unknown whether the reported changes were primary effects of bed rest or secondary effects of bed rest-induced hypovolemia. We hypothesized that restoring plasma volume with salt tablets and water after 12 days of head-down bed rest would result in an absence of hemodynamic and endocrine changes and a reduced incidence of orthostatic hypotension. In 10 men, we measured changes from pre-bed-rest to post-bed-rest in venous and arterial pressures; heart rate; stroke volume; cardiac output; vascular resistance; plasma norepinephrine, epinephrine, vasopressin, renin activity (PRA), and aldosterone responses to different tilt levels (0°, –10°, 20°, 30°, and 70°); and plasma volume and platelet 2 - and lymphocyte 2 -adrenoreceptor densities and affinities (0° tilt only). Fluid loading at the end of bed rest restored plasma volume and resulted in the absence of post-bed-rest orthostatic hypotension and changes in supine hemodynamic and endocrine variables. Fluid loading did not prevent post-bed-rest increases in 2 -adrenoreceptor density or decreases in the aldosterone-to-PRA ratio ( P = 0.05 for each). Heart rate, epinephrine, and PRA responses to upright tilt after bed rest were increased ( P < 0.05), despite the fluid load. These results suggest that incidents of orthostatic hypotension and many of the changes in supine hemodynamic and endocrine variables in volume-depleted bed-rested subjects occur secondarily to the hypovolemia. Despite normovolemia after bed rest, 2 -adrenoreceptors were upregulated, and heart rate, epinephrine, and PRA responses to tilt were augmented, indicating that these changes are independent of volume depletion. simulated microgravity; cardiovascular; hypovolemia; cardiopulmonary-arterial baroreceptor reflex interaction; adrenergic receptors
Head-down bed rest changes the values of many cardiovascular and endocrine variables and also elicits significant hypovolemia. Because previous studies had not controlled for hypovolemia, it is unknown whether the reported changes were primary effects of bed rest or secondary effects of bed rest-induced hypovolemia. We hypothesized that restoring plasma volume with salt tablets and water after 12 days of head-down bed rest would result in an absence of hemodynamic and endocrine changes and a reduced incidence of orthostatic hypotension. In 10 men, we measured changes from pre-bed-rest to post-bed-rest in venous and arterial pressures; heart rate; stroke volume; cardiac output; vascular resistance; plasma norepinephrine, epinephrine, vasopressin, renin activity (PRA), and aldosterone responses to different tilt levels (0°, −10°, 20°, 30°, and 70°); and plasma volume and platelet α 2 - and lymphocyte β 2 -adrenoreceptor densities and affinities (0° tilt only). Fluid loading at the end of bed rest restored plasma volume and resulted in the absence of post-bed-rest orthostatic hypotension and changes in supine hemodynamic and endocrine variables. Fluid loading did not prevent post-bed-rest increases in β 2 -adrenoreceptor density or decreases in the aldosterone-to-PRA ratio ( P = 0.05 for each). Heart rate, epinephrine, and PRA responses to upright tilt after bed rest were increased ( P < 0.05), despite the fluid load. These results suggest that incidents of orthostatic hypotension and many of the changes in supine hemodynamic and endocrine variables in volume-depleted bed-rested subjects occur secondarily to the hypovolemia. Despite normovolemia after bed rest, β 2 -adrenoreceptors were upregulated, and heart rate, epinephrine, and PRA responses to tilt were augmented, indicating that these changes are independent of volume depletion.
Author Mitchell, Brett M
Whitson, Peggy A
Meck, Janice V
Platts, Steven H
Waters, Wendy W
Author_xml – sequence: 1
  fullname: Waters, Wendy W
– sequence: 2
  fullname: Platts, Steven H
– sequence: 3
  fullname: Mitchell, Brett M
– sequence: 4
  fullname: Whitson, Peggy A
– sequence: 5
  fullname: Meck, Janice V
BackLink https://www.ncbi.nlm.nih.gov/pubmed/15486040$$D View this record in MEDLINE/PubMed
BookMark eNqFkdFu0zAUhi00xLrCEyAhX3HX4thJ6nCHJsaQJsHFuLZOnJPGk2MH22nXp-FVSdqNSkiIG_vifN-x_P9X5MJ5h4S8zdg6ywr-AR6GDiGkNWOcszVnLH9BFtOEr7JCVBdkwUQpVmUmiktyFeMDY6zYlOIVucyKXJYsZwvy67uF2APdeTv2SAPG5AMk4x3dm9TRCDbRBLXFFCm4hu4hYaDQzmeNzdGgQ8AduonwIXU-pmmBpt1h8AldnHfNpu7AbTFS42gcB-OQdtj75uCgn-iZQNd4HebJDoKZH42vycsWbMQ3T_eS_Lj5fH99u7r79uXr9ae7lRaVSCvZVFCItuBlLWWuN1iVutJZXUsOssozJji0stYAwJtcF22ZI4LUoqklFsjEkrw_7R2C_zlOf1K9iRqtBYd-jKrciDKrGJ_Ad0_gWPfYqCGYHsJBPUc6AeIE6OBjDNieEabm4tRzcepYnJqLm6zqL0ubdOwhBTD2P-765HZm2-1NQDV0hyl267eHs8ClVFzdyimvJfn4b-FmtPYeH9Mf8yyqoWnFb0bkzDQ
CitedBy_id crossref_primary_10_3389_fphys_2022_898430
crossref_primary_10_4236_ojneph_2013_31004
crossref_primary_10_1007_s00421_011_2083_0
crossref_primary_10_1080_02699052_2017_1408144
crossref_primary_10_1152_japplphysiol_00676_2015
crossref_primary_10_1016_j_lpm_2012_03_023
crossref_primary_10_1152_ajpheart_00802_2015
crossref_primary_10_1161_HYPERTENSIONAHA_111_172262
crossref_primary_10_1152_japplphysiol_00670_2012
crossref_primary_10_1542_peds_2017_1673
crossref_primary_10_1136_pgmj_2007_062075
crossref_primary_10_1016_j_autneu_2021_102906
crossref_primary_10_3389_fphys_2017_00603
crossref_primary_10_1016_j_jash_2011_08_008
crossref_primary_10_1097_PHM_0b013e31802b8d09
crossref_primary_10_1007_s13089_010_0033_4
crossref_primary_10_1016_j_actaastro_2010_10_008
crossref_primary_10_1177_0018720820936794
crossref_primary_10_1111_imj_13171
crossref_primary_10_3389_fphys_2019_01061
crossref_primary_10_1159_000364849
crossref_primary_10_1007_s10072_022_05963_7
crossref_primary_10_1152_ajpheart_00427_2011
crossref_primary_10_1016_j_autneu_2020_102732
crossref_primary_10_1016_j_nephro_2017_01_003
crossref_primary_10_1007_s00421_013_2787_4
crossref_primary_10_1111_j_1537_2995_2011_03202_x
crossref_primary_10_1161_HYPERTENSIONAHA_110_151787
crossref_primary_10_1152_japplphysiol_00710_2013
crossref_primary_10_1016_j_jsgi_2006_07_008
crossref_primary_10_1111_j_1442_200X_2008_02783_x
crossref_primary_10_1007_s11255_005_7663_7
crossref_primary_10_1152_japplphysiol_00019_2012
crossref_primary_10_1007_s00421_007_0474_z
crossref_primary_10_14814_phy2_13874
crossref_primary_10_1186_1742_4682_7_8
crossref_primary_10_1152_ajpheart_00391_2012
crossref_primary_10_1042_CS20110077
crossref_primary_10_1152_japplphysiol_00121_2007
crossref_primary_10_1152_ajpregu_00356_2005
crossref_primary_10_1007_s10439_010_9943_3
crossref_primary_10_1371_journal_pone_0169793
Cites_doi 10.1152/ajpheart.00740.2003
10.1016/0002-9149(86)90882-9
10.1152/jappl.1995.78.3.1023
10.1007/BF03350152
10.1152/ajpregu.1999.277.4.R1084
10.1152/jappl.1989.66.6.2778
10.1152/ajpendo.1993.265.1.E153
10.1152/jappl.1999.87.5.1614
10.1161/01.CIR.103.14.1851
10.1152/ajpheart.1989.257.5.H1389
10.1152/jappl.1990.68.4.1458
10.1152/ajpregu.1997.273.1.R93
10.1097/00006842-200111000-00003
10.1007/BF00580849
10.1126/science.3006250
10.1152/ajpregu.1994.266.6.R1962
10.1016/S0306-4530(02)00046-X
10.1097/00004872-198604000-00012
10.1016/0094-5765(94)90133-3
10.1016/S0304-3940(00)00804-1
10.1152/ajpheart.00965.2002
10.1161/01.CIR.79.1.107
10.1152/japplphysiol.00544.2001
10.1172/JCI107121
10.1152/jappl.1994.77.5.2134
10.1046/j.1365-2125.1999.00059.x
10.1152/ajpheart.00535.2001
10.1046/j.1365-2281.2001.00315.x
10.1097/00006842-199707000-00015
10.1152/ajpheart.1999.277.6.H2272
10.1016/0165-6147(87)90108-8
10.1152/jappl.1995.79.2.623
10.1097/00003246-199310000-00023
10.1152/ajpheart.1998.274.6.H1875
10.1161/01.RES.65.3.546
10.1016/S0006-291X(80)80044-1
10.1152/jappl.1998.84.2.612
10.1152/jappl.1996.81.1.7
10.1152/ajpheart.2001.280.5.H2230
10.1080/00365519109091106
10.1152/ajpregu.2000.279.6.R2189
10.1152/jappl.1996.81.1.105
10.1161/01.CIR.96.2.517
10.1210/jcem-63-4-847
10.1007/BF02267820
10.1016/S0001-2998(75)80033-X
10.1152/jappl.1996.81.5.2134
ContentType Journal Article
Contributor Meck, J V
Contributor_xml – sequence: 1
  givenname: J V
  surname: Meck
  fullname: Meck, J V
  organization: NASA JSC
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7X8
DOI 10.1152/ajpheart.00220.2004
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
DatabaseTitleList MEDLINE
MEDLINE - Academic

CrossRef
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
Anatomy & Physiology
EISSN 1522-1539
EndPage H847
ExternalDocumentID 15486040
10_1152_ajpheart_00220_2004
ajpheart_288_2_H839
Genre Research Support, U.S. Gov't, Non-P.H.S
Journal Article
GrantInformation Grant numbers: NASA NCC9-105.
GroupedDBID -
02
23M
2WC
39C
53G
5GY
5VS
8M5
ABFLS
ABPTK
ACIWK
ACPRK
ADACO
ADBBV
AENEX
AFFNX
AFRAH
ALMA_UNASSIGNED_HOLDINGS
BAWUL
BKOMP
C1A
DIK
DL
E3Z
EBS
EJD
F5P
GX1
H13
KQ8
O0-
OK1
P2P
PQEST
PQQKQ
RAP
RHF
RHI
RPL
UKR
WH7
WOQ
---
3O-
4.4
6J9
AAFWJ
AAYXX
ABJNI
ACBEA
BKKCC
BTFSW
CITATION
EMOBN
ITBOX
RPRKH
TR2
W8F
XSW
YSK
YYP
~02
CGR
CUY
CVF
ECM
EIF
NPM
7X8
ID FETCH-LOGICAL-c393t-8d9a53f526b884c7e96c9c1bb82a8941032af8bcaaa2d4c5f64eea8c3db8e5e03
ISSN 0363-6135
IngestDate Thu Jul 10 19:57:49 EDT 2025
Sat Sep 28 07:46:22 EDT 2024
Tue Jul 01 04:19:56 EDT 2025
Thu Apr 24 22:52:13 EDT 2025
Mon May 06 11:35:14 EDT 2019
Tue Jan 05 18:11:20 EST 2021
IsPeerReviewed true
IsScholarly true
Issue 2
Keywords NASA Center JSC
NASA Discipline Regulatory Physiology
Language English
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c393t-8d9a53f526b884c7e96c9c1bb82a8941032af8bcaaa2d4c5f64eea8c3db8e5e03
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
PMID 15486040
PQID 67361902
PQPubID 23479
ParticipantIDs pubmed_primary_15486040
crossref_citationtrail_10_1152_ajpheart_00220_2004
proquest_miscellaneous_67361902
highwire_physiology_ajpheart_288_2_H839
crossref_primary_10_1152_ajpheart_00220_2004
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 20050201
2005-02-00
2005-Feb
PublicationDateYYYYMMDD 2005-02-01
PublicationDate_xml – month: 02
  year: 2005
  text: 20050201
  day: 01
PublicationDecade 2000
PublicationPlace United States
PublicationPlace_xml – name: United States
PublicationTitle American journal of physiology. Heart and circulatory physiology
PublicationTitleAlternate Am J Physiol Heart Circ Physiol
PublicationYear 2005
References R21
R20
R23
R22
R25
R24
R27
R26
R29
R28
R1
R2
R3
R4
R5
R6
R7
R8
R9
R30
R32
R31
R34
R33
R36
R35
R38
R37
R39
R41
R40
R43
R42
R45
R44
R47
R46
R49
R48
R50
R52
R51
R10
R54
R53
R12
R56
R11
R55
R14
R13
R57
R16
R15
R18
R17
R19
References_xml – ident: R32
  doi: 10.1152/ajpheart.00740.2003
– ident: R5
  doi: 10.1016/0002-9149(86)90882-9
– ident: R18
  doi: 10.1152/jappl.1995.78.3.1023
– ident: R51
  doi: 10.1007/BF03350152
– ident: R48
  doi: 10.1152/ajpregu.1999.277.4.R1084
– ident: R42
  doi: 10.1152/jappl.1989.66.6.2778
– ident: R56
– ident: R54
  doi: 10.1152/ajpendo.1993.265.1.E153
– ident: R1
  doi: 10.1152/jappl.1999.87.5.1614
– ident: R39
  doi: 10.1161/01.CIR.103.14.1851
– ident: R37
  doi: 10.1152/ajpheart.1989.257.5.H1389
– ident: R9
  doi: 10.1152/jappl.1990.68.4.1458
– ident: R12
  doi: 10.1152/ajpregu.1997.273.1.R93
– ident: R31
  doi: 10.1097/00006842-200111000-00003
– ident: R26
  doi: 10.1007/BF00580849
– ident: R4
  doi: 10.1126/science.3006250
– ident: R43
– ident: R10
  doi: 10.1152/ajpregu.1994.266.6.R1962
– ident: R17
  doi: 10.1016/S0306-4530(02)00046-X
– ident: R33
  doi: 10.1097/00004872-198604000-00012
– ident: R2
– ident: R53
  doi: 10.1016/0094-5765(94)90133-3
– ident: R22
  doi: 10.1016/S0304-3940(00)00804-1
– ident: R23
  doi: 10.1152/ajpheart.00965.2002
– ident: R29
  doi: 10.1161/01.CIR.79.1.107
– ident: R55
  doi: 10.1152/japplphysiol.00544.2001
– ident: R57
  doi: 10.1172/JCI107121
– ident: R44
– ident: R13
  doi: 10.1152/jappl.1994.77.5.2134
– ident: R15
  doi: 10.1046/j.1365-2125.1999.00059.x
– ident: R24
  doi: 10.1152/ajpheart.00535.2001
– ident: R25
– ident: R34
  doi: 10.1046/j.1365-2281.2001.00315.x
– ident: R40
  doi: 10.1097/00006842-199707000-00015
– ident: R35
  doi: 10.1152/ajpheart.1999.277.6.H2272
– ident: R3
  doi: 10.1016/0165-6147(87)90108-8
– ident: R7
  doi: 10.1152/jappl.1995.79.2.623
– ident: R8
  doi: 10.1097/00003246-199310000-00023
– ident: R50
– ident: R49
  doi: 10.1152/ajpheart.1998.274.6.H1875
– ident: R19
  doi: 10.1161/01.RES.65.3.546
– ident: R20
– ident: R36
  doi: 10.1016/S0006-291X(80)80044-1
– ident: R45
– ident: R41
– ident: R47
  doi: 10.1152/jappl.1998.84.2.612
– ident: R6
  doi: 10.1152/jappl.1996.81.1.7
– ident: R38
  doi: 10.1152/ajpheart.2001.280.5.H2230
– ident: R52
  doi: 10.1080/00365519109091106
– ident: R21
  doi: 10.1152/ajpregu.2000.279.6.R2189
– ident: R27
  doi: 10.1152/jappl.1996.81.1.105
– ident: R28
  doi: 10.1161/01.CIR.96.2.517
– ident: R14
  doi: 10.1210/jcem-63-4-847
– ident: R11
  doi: 10.1007/BF02267820
– ident: R46
  doi: 10.1016/S0001-2998(75)80033-X
– ident: R16
  doi: 10.1152/jappl.1996.81.5.2134
– ident: R30
SSID ssj0005763
Score 2.0177026
Snippet 1 Human Adaptation and Countermeasures Office, Wyle Laboratories, Inc.; 2 Division of Space Life Sciences, Universities Space Research Association; and 3...
Head-down bed rest changes the values of many cardiovascular and endocrine variables and also elicits significant hypovolemia. Because previous studies had not...
SourceID proquest
pubmed
crossref
highwire
SourceType Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage H839
SubjectTerms Adult
Aldosterone - blood
Baroreflex - physiology
Bed Rest - adverse effects
Blood Pressure - physiology
Drinking
Endocrine System - physiology
Epinephrine - blood
Heart Rate - physiology
Humans
Hypotension, Orthostatic - etiology
Hypotension, Orthostatic - physiopathology
Hypotension, Orthostatic - prevention & control
Male
Norepinephrine - blood
Plasma Volume - physiology
Receptors, Adrenergic - physiology
Renin - blood
Sodium Chloride - administration & dosage
Space Flight
Stroke Volume - physiology
Supine Position
Vascular Resistance - physiology
Vasopressins - blood
Weightlessness Simulation - adverse effects
Title Plasma volume restoration with salt tablets and water after bed rest prevents orthostatic hypotension and changes in supine hemodynamic and endocrine variables
URI http://ajpheart.physiology.org/cgi/content/abstract/288/2/H839
https://www.ncbi.nlm.nih.gov/pubmed/15486040
https://www.proquest.com/docview/67361902
Volume 288
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Lj9MwELbKIiEuK9jl0eXlA4JDyZJ1HuscVwhUgYqK1BV7ixzHWYq2SdS6i8qf4X_xa5ixnQfQRcAlqhI7TjNf7JnxzDeEPGV-AcpQoDx2zHIv5InwEliFPaZy3FWSRXiEycmT9_H4NHx7Fp0NBt97UUtrnR3Kr1vzSv5HqnAO5IpZsv8g2famcAJ-g3zhCBKG41_JeAqq70KM7AwzWpoiMVagNvJcXOiRxtwobZmYvwikRLRlwTOVmx7IEnBp0txwB6fCBCOkvd7UlYltd8HKNj_YxM6u1jVqpp_UosptOXvTQpV5JTGVcHQJ5jcOuuorvu3OUI-qwnhVjFv_ENOhljbYXc6XGBtrNv-7Fp3jX7uqbh9hxM2odRHBu9B65QLX4A91WReTuTbhrhbKSuvOA4zlAV3K2VSdn2-cZ7fxgkRN4HTRZX8FYAZb6pNmZmec9yDMevP0mFsKpd8XkAgJacXnGuuJa3S3Md94EfqtAQX1wmAKDb7Yt4RTv_B2N5eukesMTBgsK_LuQ8dkD3Ze0Oyj43M7RiwY_-WW0U31KHu_nxWohtT6agPJKEqzW2TXWTj0xML1Nhmoco_sn5Qg0cWGPqPTVqZ75MbEhXbsk28WzNS-VNoDM0UwUwQzdWCmgBNqwEwNmCmA2fSgDZhpD8y0B2bT04GZzktqwUx7YDYtWjDTFsx3yOmb17NXY89VD_FkkATa43kioqCIWJxxHspjlcQykUdZxpngSYhEkqLgmRRCsDyUURGHSgkugzzjKlJ-cJfslFWp7hOahAI6Bj6Tfh7GfpBJxiNfiZDDLBeLbEhYI5JUOmp9rPBykRoTO2JpI9LUiBRrv4ZD8qLtVFtmmT83DxpZp93Hl6KjagbAa7sA5lOWIr7TOi-G5Pm2Xu39u9ZD8qQBUAorDG4bilJV65WJ_ASzgQ3JPYur7nEdJA-uvPKA3Oy-1odkRy_X6hFo8Tp7bD6HH1sEAA0
linkProvider Colorado Alliance of Research Libraries
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Plasma+volume+restoration+with+salt+tablets+and+water+after+bed+rest+prevents+orthostatic+hypotension+and+changes+in+supine+hemodynamic+and+endocrine+variables&rft.jtitle=American+journal+of+physiology.+Heart+and+circulatory+physiology&rft.au=Waters%2C+Wendy+W&rft.au=Platts%2C+Steven+H&rft.au=Mitchell%2C+Brett+M&rft.au=Whitson%2C+Peggy+A&rft.date=2005-02-01&rft.issn=0363-6135&rft.volume=288&rft.issue=2&rft.spage=H839&rft_id=info:doi/10.1152%2Fajpheart.00220.2004&rft_id=info%3Apmid%2F15486040&rft.externalDocID=15486040
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0363-6135&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0363-6135&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0363-6135&client=summon