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Danish Aerospace Medical Centre of Research, Rigshospitalet 7805, DK-2200 Copenhagen, Denmark
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump,
and Peter Norsk. Contribution of abdomen and legs to central blood
volume expansion in humans during immersion. J. Appl.
Physiol. 83(3): 695-699, 1997.
The hypothesis was
tested that the abdominal area constitutes an important reservoir for
central blood volume expansion (CBVE) during water immersion in
humans. Six men underwent 1) water immersion for 30 min (WI),
2) water immersion for 30 min with
thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs
from contributing to CBVE (WI+Occl), and
3) a seated nonimmersed control with
15 min of thigh cuff inflation (Occl). Plasma protein concentration and
hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4%
(P < 0.05), respectively, during WI
but were unchanged during WI+Occl. Left atrial diameter increased from
27 ± 2 to 36 ± 1 mm (P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm (P < 0.05). Central
venous pressure increased from 
3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI (P < 0.05) but
only increased to 7.0 ± 0.8 mmHg during WI+Occl
(P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the
legs, whereas the CBVE is caused mainly by blood from the
abdomen.
blood proteins; echocardiography; atrium; central venous pressure; blood pressure
INTRODUCTION THERMONEUTRAL (34.5°C) water immersion (WI) to the
neck in humans induces central blood volume expansion (CBVE) with
increases in central venous pressure (CVP) (1, 4, 7, 10, 13, 14, 19,
20), cardiac output (1, 14, 20), heart volume (12, 19), and left atrial
diameter (LAD) (18). In addition to these changes, we and
others have previously shown that blood is diluted during WI, resulting
in an increase in plasma volume and a decrease in plasma protein
concentration (Pprot),
colloid osmotic pressure (COP), and hematocrit (Hct)
(8-11, 13).
We have previously observed that the WI-induced hemodilution is caused
mainly by transfer of fluid from the interstitial compartment of the
legs to the intravascular space (10). By immersing subjects to the
hips, hemodilution of almost similar magnitude as that of immersion to
the neck was induced with only a small temporary increase in CVP. Only
by immersing the subjects to the neck did the major increase in CVP
occur (10).
That CVP in our previous study only increased during neck immersion and
not during immersion to the hips is not final evidence that the region
above the legs is the only contributor to CBVE. The increased
hydrostatic pressure during neck compared with during hip immersion
might facilitate further translocation of some blood and fluid from the
legs to the intrathoracic circulation in combination with transfer of
blood from the abdominal region. Thus the contribution to CBVE from the
abdomen and legs during neck immersion remains unclear.
To investigate the importance of fluid and blood reservoirs of the legs
vs. those of the intra-abdominal region for the WI-induced CBVE, we
performed a study during which the thighs were totally occluded by
inflation of cuffs of 250 mmHg for 15 min during seated WI to the neck.
It has previously been shown that a cuff pressure of 240 mmHg is
sufficient to occlude blood flow to the lower limbs during immersion
(17). In this manner, the legs were prevented from contributing to the
WI-induced CBVE and hemodilution. Thus the hypothesis was tested that
the abdominal area constitutes an important reservoir of blood and
fluid for CBVE during WI in humans.
MATERIALS AND METHODS Six healthy men [age 24 ± 1 (SE) yr, weight 85 ± 5 kg,
and height 1.89 ± 0.03 m] participated in the experiment. All
had a negative history of cardiovascular or kidney diseases and
exhibited normal results at routine clinical examination, including
measurement of blood hemoglobin concentration (Hb), arterial blood
pressure, test-strip-based urinalysis, and electrocardiogram
(ECG). All subjects denied taking any medication at the
time of the study. The experimental protocol was approved by the
Ethical Committee of Copenhagen (01-060/96), and after careful oral and
written explanation, written consent was obtained according to the
Declaration of Helsinki.
Each subject underwent three experimental sessions in the upright
seated posture with the sequence in a balanced order between the
subjects on the same study day separated by at least 1.5 h: 1) WI to the neck for 30 min,
2) WI to the neck for 30 min with thigh cuff inflation of 250 mmHg during the initial 15 min (WI+Occl), and 3) a seated control for 30 min
outside the water with thigh cuff inflation of 250 mmHg during the
initial 15 min (Occl). Each session was preceded and followed by the
subjects being seated outside the water for 1.5 and 0.5 h,
respectively. The control period of 30 min after an experimental
session also constituted the initial part of the subsequent control
period of 1.5 h. The duration of the entire experimental sequence was
6.5 h. No food or fluid intake was allowed during the final 12 h before
the beginning of the experiment.
From 10:00 PM the evening before the experiment, the subject was
confined to the laboratory. He was awakened at 7:00 AM. With local skin
anesthesia and continuous ECG monitoring, a polyethylene central venous
catheter (Cavafix, Braun) was inserted through an antecubital vein into
the intrathoracic region for measurements of CVP and collection of
blood. Intrathoracic placement of the central venous catheter was
confirmed by typical CVP waveforms and responses to respiratory
maneuvers. After emptying his bladder, the subject drank 400 ml of tap
water and was weighed and then seated upright wearing a bathing suit in
a chair outside the WI tank for 1.5 h. Thereafter, he was subjected to
WI, WI+Occl, or Occl. At all times during the experiment (before,
during, and after immersion), both of the subject's arms were kept
resting on a support and always at the same distance above heart level.
Arterial pressures [systolic (SAP), diastolic (DAP), mean (MAP)],
CVP, heart rate (HR), and LAD were determined every 5 min during WI,
Occl, and WI+Occl and every 15 min before and after the
interventions. Five milliliters of blood for determination of Hct, Hb, Pprot, plasma density
(PD), and COP were sampled at the same experimental points in time from
the central venous catheter. Before each blood sampling, 2 ml of blood
were drawn to empty dead space. The total amount of collected blood
from each subject was 230 ml. After each sampling of blood, the
catheter was flushed with an amount of saline equal to that of the
collected blood. The subject stood briefly on the chair to void at an
hourly interval (immediately before an intervention and at the end of
the 30-min postintervention control period after completion of the
measurements) and drank 200 ml of water immediately
afterward. The reason for having the subject void and
drink was to maintain the same hydration protocol as during previous WI
studies in which renal function was assessed (10, 11, 13, 20).
Procedures were always performed in the following sequence: blood
sampling and measurements of arterial pressures, CVP, HR, and LAD.
WI was carried out in tap water in a rectangular insulated plastic tank
with an adjustable chair suspended from the ceiling in an electrical
hoist. WI was performed by lowering the chair with the subject into the
water. During the control periods outside the water, the subject sat in
the chair above the water surface. Water and air temperatures were
measured every 0.5 h with mercury thermometers, and air humidity was
determined with a hygrometer. The average water temperature varied over
time between 34.67 ± 0.04 and 34.82 ± 0.04°C (SE), room
temperature between 25.2 ± 0.2 and 26.0 ± 0.1°C, and
relative air humidity between 35 ± 2 and 41 ± 1%.
At the beginning of the experiment, a standard-size thigh cuff (20 × 88 cm) was placed around each thigh of the subject as close to
the genitofemoral region as possible. Immediately before start of Occl
or WI+Occl, the cuffs were manually inflated to a pressure of 250 mmHg
within 60 s. After inflation of the cuffs, the subject was either
lowered into the water within 15 s (WI+Occl) or remained seated outside
the water (Occl). During WI, the cuffs remained around the thighs of
the subject without being inflated. In all subjects, occlusion of blood
flow to the legs induced only minor discomfort in the form of a
"cotton wool" sensation in the legs. The discomfort vanished
immediately after deflation of the cuffs.
Blood samples were transferred to polyethylene tubes containing 12.5 IU
heparin/ml blood. The samples were centrifuged at 4°C for 10 min at
1,500 g, and immediately afterward the
plasma was analyzed for Pprot and
PD. Plasma samples for determination of COP were maintained cooled at
4°C and were analyzed within 1 wk.
Hct was measured in quadruplicate by centrifugation of microhematocrit
tubes in a centrifuge for 5 min at 15,000 g. Hct values were not corrected for
trapped plasma and whole body Hct. Hb in blood was measured in
duplicate by a spectrophotometric method as described previously
(11).
Pprot was measured in duplicate in
a refractometer (pocket refractometer, Bellingham & Stanley). PD was
determined in a density meter (model DMA 46, Paar) with an accuracy of
1 × 10 For measurements of CVP, the central venous catheter was connected to a
disposable pressure transducer (model DTXX, Viggo-Spectramed). The
reference level for the CVP measurements was chosen at the sternal
border of the fourth intercostal space. After amplification, the
pressure signal was displayed on a strip chart produced by an
electrostatic recorder (model ES 1000, Gould). Electronic mean values
were used for estimation of CVP.
LAD was measured by M-mode echocardiography (Aloka SSD 500, Simonsen & Weel). Standard images were obtained from the parasternal long axis
view during the end-expiratory phase of respiration and recorded on a
video recorder. LAD was then determined by an independent observer from
an average of three printouts from the recorder according to Feigenbaum
(6).
HR was calculated as the mean value over a minimum period of 30 s from
ECG recordings obtained simultaneously with CVP from electrodes on the
subject's shoulders and head and connected to an oscilloscope
(Diascope DS 521, Simonsen & Weel) and a strip-chart recorder (model ES
1000, Gould).
SAP and DAP were measured over a brachial artery with an automatic
oscillometric equipment (Propaq 102, Dameca) with the arm resting 20 cm
above heart level on all occasions before, during, and after WI,
WI+Occl, and Occl to prevent the arms from being immersed. Therefore,
SAP, DAP, and MAP are ~15 mmHg lower than usually observed. Arterial
pulse pressure (PP) was calculated from SAP Measurements of body weight were performed before the start of the
experiment on an electronic scale (Detecto, Simonsen & Weel).
Data are presented as means ± SE. A multifactorial analysis of
variance [(ANOVA); Statgraphics Plus for Windows, version
2.0] for repeated measures with the variable as the main variate
and time and subjects as factors was used to evaluate the effects on a
variable over time within each series of experiment (WI, WI+Occl, and
Occl). To evaluate the effect of each intervention at the
same experimental point in time, an ANOVA for repeated measures was
used with the variable as the main variate and intervention (WI,
WI+Occl, and Occl) and subjects as factors. Differences
between mean values were evaluated by a post hoc multiple-range test
(Newman-Keuls). A significance level of 0.05 was chosen.
RESULTS
4
g/ml. COP was measured in duplicate in a colloid osmometer (model 4400, Wescor).
DAP, and MAP was
calculated from DAP + 
PP.
Fig. 1.
Plasma protein concentration (Pprot;
A), plasma density (PD; B), and plasma
colloid osmotic pressure (COP; C) before, during, and
after 30 min of water immersion (WI; 
), water immersion for 30 min
with occlusion of thighs with 250 mmHg during initial 15 min (WI+Occl;
), and seated control for 30 min with occlusion of thighs with 250 mmHg for 15 min (Occl; 
). Values are means ± SE of 6 subjects
for Pprot and PD and of 5 subjects for COP. # Significant difference compared with
preimmersion and preocclusion values, P < 0.05. @ Significant difference compared with values
at similar points in time during Occl and WI+Occl, P < 0.05.
[View Larger Version of this Image (22K GIF file)]
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), WI+Occl (),
and Occl (). Values are means ± SE of 6 subjects.
# Significant difference
compared with preimmersion and preocclusion values,
P < 0.05. @ Significant difference
compared with values at similar points in time during Occl and WI+Occl,
P < 0.05.
During WI, CVP (Fig. 2) increased within 5 min from
3.7 ± 1.0 to
10.4 ± 0.8 mmHg (P < 0.05) and
remained at this level during the entire immersion period. In contrast
to this, CVP increased from 3.8 ± 0.6 to only 7.0 ± 0.8 mmHg
(P < 0.05) during WI+Occl. It
further increased after cuff deflation to 9.6 ± 0.8 mmHg
(P < 0.05). No changes were observed
during Occl.
MAP (Fig. 2) was unchanged during WI but increased from 75 ± 3 mmHg
to between 88 ± 3 and 90 ± 2 mmHg during the inital 15 min of
WI+Occl (P < 0.05). After cuff
deflation, values returned to the Occl and WI levels. No changes
occurred during Occl. The increase in MAP during WI+Occl was due to an
increase in both SAP and DAP (Table 2;
P < 0.05). PP (Table
2) increased at the end of WI compared with the values of Occl and
Occl+WI at the same experimental point in time
(P < 0.05) but was unchanged during WI+Occl and Occl.
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DISCUSSION
The decreases in Pprot, PD, COP, Hct, and Hb during the initial 15 min of WI were similar in magnitude to those observed previously in dogs (15) and humans (8-11, 13). The fact that these variables were unchanged during WI+Occl supports the concept that the interstitial compartment of the legs is the main reservoir for the WI-induced hemodilution. These results agree with those of Miki et al. (16), who demonstrated in dogs that a more negative transcapillary pressure gradient develops in the legs during WI. If it is anticipated that a similar negative gradient develops in humans, this would facilitate flow of protein-poor fluid from the interstitial to the intravascular compartment of the legs and thereby induce the observed decreases in Pprot, PD, and COP. Therefore, the development of a negative transcapillary pressure gradient induces hemodilution during WI and apparently overrides the opposing effects of the WI-induced peripheral vasodilatation in the legs (20).
Because LAD increased to a similar extent during WI with or without occlusion of the thighs, the major reservoir of blood for CBVE must have been located above the legs. The further increase in CVP on release of the cuff pressure during WI+Occl indicates that the additional fluid from the legs, causing hemodilution, was sufficient to further increase intracardiac pressures. That this was not reflected in a measurable increase in LAD could be due to the fact that CBVE during the initial 15 min of WI+Occl was of such a magnitude that the intracardiac volume-pressure relationship operated on the flat slope of the Starling curve with a reduced cardiac compliance.
WI has been used over the past decades as an analog of weightlessness (microgravity during spaceflight). The indication of a reduced cardiac compliance during WI is apparently in contrast to results from space where microgravity-induced increases in cardiac chamber dimension in the presence of reduced CVP were observed (3). Thus WI as an analog of microgravity in regard to cardiac compliance should be further evaluated.
The increase in MAP during the initial 15 min of Occl+WI indicates that the vascular bed in the legs is important for maintaining MAP unchanged during WI (7, 13). Because cardiac output increases during WI (1, 14, 20), inability of the resistance vessels to vasodilate during WI+Occl might have induced an increase in afterload and thereby in MAP during WI+Occl. Cardiac output, however, was not measured during this experiment, and, therefore, this hypothesis remains speculative.
When blood flow to a limb is occluded, arterial blood pressure, presumably through a chemoreceptor reflex, has been shown to increase. This reflex is augmented during exercise (2). We did not observe a significant increase in MAP during 15 min of Occl. The apparent "noisiness," as indicated by the large fluctuations in MAP, during Occl indicates that inflation of the cuffs could have had an effect on at least some of the subjects.
In conclusion, the results indicate that fluid shift from the interstitial to the intravascular space in the legs constitutes the source of hemodilution during WI, whereas the most important reservoir of blood causing CBVE is located in the abdomen. The legs might also be important for maintaining MAP unchanged. Thus there is a dissociation between the importance of the two vascular beds in regard to the WI-induced hemodilution and CBVE, respectively.
Because both CBVE and hemodilution are considered stimuli for the natriuresis and diuresis of WI in humans (5, 10), it should in the future be attempted to separate the effects of the two on kidney function. Thus WI studies should be conducted in which COP is kept unchanged to more accurately assess the relative importance of this variable for renal function in humans.
ACKNOWLEDGEMENTS
The helpful comments of Peter Bie and the technical assistance of Jonas Hink are gratefully acknowledged.
FOOTNOTES
Address for reprint requests: P. Norsk, Danish Aerospace Medical Centre of Research, Rigshospitalet 7805, 20 Tagensvej, DK-2200 Copenhagen, Denmark.
Received 2 October 1996; accepted in final form 22 April 1997.
REFERENCES
| 1. | Arborelius, M., Jr., U. I. Balldin, B. Lilja, and C. E. G. Lundgren. Hemodynamic changes in man during immersion with the head above water. Aerospace Med. 43: 592-598, 1972[Medline]. |
| 2. |
Bonde-Petersen, F.,
L. B. Rowell,
R. G. Murray,
C. G. Blomqvist,
R. White,
E. Karlsson,
W. Campbell,
and
J. H. Mitchell.
Role of cardiac output in the pressor responses to graded muscle ischemia in man.
J. Appl. Physiol.
45:
574-580,
1978 |
| 3. |
Buckey, J. C., Jr.,
F. A. Gaffney,
L. D. Lane,
B. D. Levine,
D. E. Watenpaugh,
S. J. Wright,
C. W. Yancy, Jr.,
D. M. Meyer,
and
C. G. Blomqvist.
Central venous pressure in space.
J. Appl. Physiol.
81:
19-25,
1996 |
| 4. | Echt, M., L. Lange, and O. H. Gauer. Changes of peripheral venous tone and central transmural venous pressure during immersion in a thermoneutral bath. Pflügers Arch. 352: 211-217, 1974[Medline]. |
| 5. |
Epstein, M.
Renal effects of head-out water immersion in humans: a 15-year update.
Physiol. Rev.
72:
563-621,
1992 |
| 6. | Feigenbaum, H. Echocardiography (5th ed.). Philadelphia, PA: Lea & Febiger, 1994. |
| 7. |
Gabrielsen, A.,
L. B. Johansen,
and
P. Norsk.
Central cardiovascular pressures during graded water immersion in humans.
J. Appl. Physiol.
75:
581-585,
1993 |
| 8. |
Greenleaf, J. E.,
J. T. Morse,
P. R. Barnes,
J. Silver,
and
L. C. Keil.
Hypervolemia and plasma vasopressin response during water immersion in men.
J. Appl. Physiol.
55:
1688-1693,
1983 |
| 9. | Greenleaf, J. E., E. Shvartz, and L. C. Keil. Hemodilution, vasopressin suppression, and diuresis during water immersion in man. Aviat. Space Environ. Med. 52: 329-336, 1981[Medline]. |
| 10. |
Johansen, L. B.,
P. Bie,
J. Warberg,
N. J. Christensen,
and
P. Norsk.
Role of hemodilution on renal responses to water immersion in humans.
Am. J. Physiol.
269 (Regulatory Integrative Comp. Physiol. 38):
R1068-R1076,
1995 |
| 11. |
Johansen, L. B.,
N. Foldager,
C. Stadeager,
M. S. Kristensen,
P. Bie,
J. Warberg,
M. Kamegai,
and
P. Norsk.
Plasma volume, fluid shifts, and renal responses in humans during 12 h of head-out water immersion.
J. Appl. Physiol.
73:
539-544,
1992 |
| 12. | Lange, L., S. Lange, M. Echt, and O. H. Gauer. Heart volume in relation to body posture and immersion in a thermoneutral bath. A roentgenometric study. Pflügers Arch. 352: 219-226, 1974[Medline]. |
| 13. |
Larsen, A. S.,
L. B. Johansen,
C. Stadeager,
J. Warberg,
N. J. Christensen,
and
P. Norsk.
Volume-homeostatic mechanisms in humans during graded water immersion.
J. Appl. Physiol.
77:
2832-2839,
1994 |
| 14. | Löllgen, H., G. V. Nieding, K. Koppenhagen, F. Kersting, and H. Just. Hemodynamic response to graded water immersion. Klin. Wochenschr. 59: 623-628, 1981[Medline]. |
| 15. | Miki, K., G. Hajduczok, S. K. Hong, and J. A. Krasney. Plasma volume changes during head-out water immersion in conscious dogs. Am. J. Physiol. 251 (Regulatory Integrative Comp. Physiol. 20): R582-R590, 1986. |
| 16. |
Miki, K.,
M. R. Klocke,
S. K. Hong,
and
J. A. Krasney.
Interstitial and intravascular pressures in conscious dogs during head-out water immersion.
Am. J. Physiol.
257 (Regulatory Integrative Comp. Physiol. 26):
R358-R364,
1989 |
| 17. |
Mittleman, K. D.,
and
I. B. Mekjavic.
Effect of occluded venous return on core temperature during cold water immersion.
J. Appl. Physiol.
65:
2709-2713,
1988 |
| 18. |
Myers, B. D.,
C. Peterson,
C. Molina,
S. J. Tomlanovich,
L. D. Newton,
R. Nitkin,
H. Sandler,
and
F. Murad.
Role of cardiac atria in the human renal response to changing plasma volume.
Am. J. Physiol.
254 (Renal Fluid Electrolyte Physiol. 23):
F562-F573,
1988 |
| 19. | Risch, W., H. J. Koubenec, U. Beckmann, S. Lange, and O. H. Gauer. The effect of graded immersion on heart volume, central venous pressure, pulmonary blood distribution, and heart rate in man. Pflügers Arch. 374: 115-118, 1978[Medline]. |
| 20. |
Stadeager, C.,
L. B. Johansen,
J. Warberg,
N. J. Christensen,
N. Foldager,
P. Bie,
and
P. Norsk.
Circulation, kidney function, and volume-regulating hormones during prolonged water immersion in humans.
J. Appl. Physiol.
73:
530-538,
1992 |
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