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1 Department of Aviation Medicine, The Heart Centre, Copenhagen University Hospital 7522; 2 Department of Clinical Physiology, Copenhagen University Hospital 4012; 4 Department of Medical Physiology, The Panum Institute, DK-2100 Copenhagen; and 3 Department of Internal Medicine and Endocrinology, Herlev Hospital, University of Copenhagen, DK-2730 Herlev, Denmark
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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The hypothesis was tested that changing
the direction of the transverse gravitational stress in horizontal
humans modulates cardiovascular and renal variables. On different study
days, 14 healthy males were placed for 6 h in either the
horizontal supine or prone position following 3 h of being supine.
Eight of the subjects were in addition investigated in the horizontal
left lateral position. Compared with supine, the prone position
slightly increased free water clearance (349 ± 38 vs. 447 ± 39 ml/6 h, P = 0.05) and urine output (1,387 ± 55 vs. 1,533 ± 52 ml/6 h, P = 0.06) with no
statistically significant effect on renal sodium excretion (69 ± 3 vs. 76 ± 5 mmol/6 h, P = 0.21). Mean arterial pressure and left atrial diameter were similar comparing effects of
supine with prone. The prone position induced an increase in heart rate
(54 ± 2 to 58 ± 2 beats/min, P < 0.05),
total peripheral vascular resistance (13 ± 1 to 16 ± 1 mmHg · min
1 · l1,
P < 0.05), forearm venous plasma concentration of
norepinephrine (97 ± 9 to 123 ± 16 pg/ml, P < 0.05), and atrial natriuretic peptide (49 ± 4 to 79 ± 12 pg/ml, P < 0.05), whereas stroke volume decreased (122 ± 5 to 102 ± 3 ml, P < 0.05, n = 6). The left lateral position had no effect on
renal variables, whereas left atrial diameter increased (32 ± 1 to 35 ± 1 mm, P < 0.05) and mean arterial
pressure decreased (90 ± 2 to mean value of 85 ± 2 mmHg,
P < 0.05). In conclusion, the prone position reduced
stroke volume and increased sympathetic nervous activity, possibly
because of mechanical compression of the thorax with slight impediment
of arterial filling. The mechanisms of the slightly augmented urine
output in prone position require further experimentation.
blood pressure; diuresis; gravitation; natriuresis
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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IT IS WELL KNOWN that a change in posture along the z-axis (long axis) of the human body has a pronounced effect on cardiovascular, endocrine, and renal variables (20). A 12-h posture change in humans from upright seated to 3° head-down tilt induces an increase in central blood volume with a simultaneous decrease in arterial pressures (23). Furthermore, renal sodium excretion (UNaV), urine flow rate (V), and solute free water clearance (CH2O) increase within the initial 3-4 h of the antiorthostatic posture change, and plasma concentrations of norepinephrine (NE) and aldosterone and plasma renin activity (PRA) decrease. These effects are thought to be initiated by the increase in central blood volume through neuroendocrine reflexes. Thus a decrease in gravitational stress (G-stress) along the z-axis of the human body (Gz) leads to depletion of fluid and electrolytes.
It is noteworthy that the effects of changing the Gz-stress on cardiovascular, endocrine, and renal variables have been thoroughly investigated (3, 20, 26), whereas the effects of changing the transverse G-stress (front to back or back to front: ±Gx; right to left or left to right: ±Gy) in horizontal healthy humans are virtually unknown. Some investigations in this regard have been initiated as a consequence of operational objectives in aerospace medicine, where G-forces higher than one have usually been used (27, 29-31).
In 1935, Wood and Wolferth (34) already described the phenomenon that some cardiac patients tolerate one recumbent position better than another, but they failed to show the underlying mechanisms. In a recent study, Fujita et al. (11) observed that patients with chronic heart failure and increased sympathetic nervous activity prefer to lie in lateral positions when recumbent, where the plasma concentration of NE decreases compared with that of the supine position. Although some authors demonstrated that cardiac output (CO) increases in horizontal lateral positions in critically ill patients and dogs and pigs (1, 5, 19, 33), others have not observed significant changes (7, 12, 17). Thus observations regarding the cardiovascular effects of changing the transverse G-stress in humans are conflicting and few.
We therefore tested the hypothesis that changing the direction of the transverse G-stress in humans modulates cardiovascular, endocrine, and renal variables. It was thought that these horizontal posture changes would induce different degrees of mechanical compression of the thorax with subsequent effects on central blood volume and renal sodium and water handling.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Fourteen healthy male subjects [age 25.0 ± 0.6 yr (means ± SE), height 181 ± 1 cm, and weight 76 ± 2 kg] completed the protocol. All had a negative history of cardiovascular and kidney diseases and were healthy as indicated by results of a questionnaire similar to the one of class 1 examination of professional pilots, a physical examination by a physician, hematocrit (0.35-0.50), arterial pressures (<140/90 mmHg), electrocardiogram (unipolar), and urine tests (strips) for glucose, leukocytes, erythrocytes, and protein. None of the subjects took any medication at the time of study. Informed consent was obtained after the subjects had read a description of the experimental protocol, which was approved by the Ethics Committee of Copenhagen (KF 01-090/95) and was in compliance with the declaration of Helsinki. Two additional subjects originally entered the study but were later excluded due to occurrence of vasovagal syncope and back pain. No other complications occurred.
For 4 days before each experimental day, the subject ingested standardized meals containing 135 mmol sodium per 24 h. In this period, he was only allowed to drink tap water and was instructed to drink in excess to avoid thirst. For 24 h before the experiment, the subject collected all urine in a plastic container for determination of 24-h sodium output.
The subject fasted for 12 h before the experiment, spent the night at the laboratory, and was awakened at 7 AM. A short catheter (Venflon 2, 1.2 mm, length 45 mm) was inserted into a cubital vein for blood sampling, and an inflatable cuff was placed around an upper arm for determination of arterial pressures. The subject rested supine for 30 min before the start of the experiment at 8 AM.
The experiment consisted of 2 experimental days of 9 h each performed in a randomized balanced sequence among the subjects and separated by at least 18 days. During each experiment, the subject was placed horizontally on a foam rubber mattress. For the initial 3 h, he was lying in the horizontal supine position on the back (preintervention) followed by 6 h of being placed in either the same supine position (Supine) or in the horizontal prone (Prone) position.
At the start of the experiment and thereafter at 1.5-h intervals, blood was sampled, arterial pressures and heart rate (HR) were measured, and urine was collected by having the subjects briefly stand up beside the bed during voiding. The subjects drank 400 ml of water initially at 8 AM and were thereafter kept hydrated with 300 ml each 1.5 h. The procedures were always performed in the following sequence: blood sampling, determination of arterial pressures, HR, collection of urine, and, finally, oral intake of water.
Systolic (SAP) and diastolic arterial pressures (DAP) were measured in
a brachial artery by an automatic oscillometric method in
n = 8 (Propac 102, Dameca, Denmark) or by auscultation
and sphygmomanometry in n = 6. Arterial pulse pressure
(PP) was calculated from SAP 
DAP and mean arterial pressure
(MAP) from DAP + 1/3 PP. The cuff around the upper arm was kept
alongside the body. HR was measured over 1 min by manually palpating
the radial artery.
Left atrial diameter was measured at end systole (n = 8) according to the criteria of Feigenbaum (8) during end-expiration from 3 M-mode printouts on a video recorder (Sony SVO-9500 MDP) obtained from the parasternal long-axis view by echocardiography (Aloka SSD 500, Simonsen & Weel). In Prone, the echocardiographic measurements were performed through a hole in the mattress, on which the subject was placed.
Twenty-seven milliliters of blood were sampled from the peripheral
venous catheter each 1.5 h and immediately transferred to chilled
tubes, and the catheter was thereafter flushed with 25-30 ml of
isotonic saline. Samples for determinations of plasma concentrations of
NE and epinephrine (E) were transferred to polyethylene tubes
containing 20 µl/ml blood of a mixture of reduced glutathione and
EGTA (0.195 mol/l glutathione, 0.250 mol/l EGTA) adjusted to pH
6-7 with NaOH. Those for vasopressin determinations
contained 41 µmol K2EDTA and those for atrial natriuretic
peptide (ANP) determinations contained 12 µmol K2EDTA and
75 µl trasylol (500 kallikrein inactivator U/ml blood; Trasylol,
Bayer, Leverkusen, Germany). The tubes for determination of
plasma concentration of aldosterone, PRA, and plasma osmolality,
respectively, contained 15 ± 2.5 IU lithium-heparin/ml blood. The
samples were immediately placed on ice and subsequently centrifuged at
4°C at 1,500 g for 10 min. Plasma was thereafter
transferred to polyethylene tubes and frozen at 30°C for later
analysis, except for the plasma for determination of osmolality, which
was measured on fresh samples by freezing-point depression (Advanced
Instruments 3MO plus). Plasma concentrations of NE and E were measured
by a radioenzymatic assay (16), vasopressin and ANP by
radioimmunoassays as previously described (15, 28),
aldosterone by use of a commercial kit (Coat a count, Diagnostics
Products, Los Angeles, CA), and PRA by use of the antibodytrapping
method as described by Poulsen and Jørgensen (24).
The exact time of end of voiding was noted and urine volume was measured in measuring glasses. Concentrations of sodium and potassium were determined in fresh urine with an ion-selective electrode method (KNA-2, Radiometer, Copenhagen, Denmark), and urine osmolality (Uosm) was measured by freezing-point depression as described above. V, UNaV, potassium excretion (UKV), osmotic excretion (UosmV), and solute CH2O were calculated by conventional formulas. Room temperature was kept between 23.2 and 26.7°C and humidity between 12 and 47%.
In six of the subjects, another catheter (Venflon 2, 1.2 mm, length 45 mm) was inserted into the contralateral cubital vein for infusion of 51Cr-EDTA (Cr-51). At 7:30 AM after sampling of blood, a bolus infusion of 18 ml solution containing 30 MBq Cr-51 in 500 ml isotonic saline was given, and thereafter it was infused at a rate of 20 ml/h throughout the experiment. Glomerular filtration rate (GFR) was measured by renal plasma clearance of Cr-51, and fractional sodium excretion (FENa) was calculated by conventional formula. A total of 23 MBq Cr-51 was infused on each experimental day.
CO was measured (n = 6) by rebreathing inert blood-soluble (N2O) and -insoluble (SF6) gases, which were analyzed by a photo- and magnetoacoustic multigas analyzer (AMIS 2001, Innovision A/S, Odense, Denmark) (4). Pulmonary blood flow = CO was calculated from the disappearence rate of the blood-soluble tracer gas, N2O, corrected for system volume changes, which were estimated by concentration changes in the blood-insoluble gas, SF6 (4). The rebreathing procedure was practiced before the start of the experiment, and CO was measured at 1.5-h intervals. Total peripheral vascular resistance and stroke volume were calculated from MAP/CO and CO/HR, respectively.
Additional study. Eight of the subjects were on an additional study day investigated in the horizontal left lateral position (Lateral). The same measurements (except for CO, hormones, and GFR) were performed. In Lateral, the pressure cuff for arterial pressure determinations was kept alongside the body and thus above heart level. Therefore, in Lateral, the vertical distance between midcuff level and the aortic valves (the latter determined by echocardiography) was measured, and the hydrostatic pressure corresponding to this distance was added to the recorded brachial arterial pressures (18).
An ANOVA (Statgraphics plus for Windows, version 3.0) for repeated measures with the variable as main variate and time and subject as factors was used to evaluate the effects on a variable over time within each series of experiment. To detect whether values of the three series differed significantly over the same experimental periods, an ANOVA was used with position (Supine, Prone, and Lateral) and subjects as factors. Differences between mean values were evaluated by a post hoc multiple range test (Newman-Keuls or least significant difference when indicated). A paired Student's t-test was used to detect whether means differed at selected points in time of two sessions. Logarithmic transformation of data was performed before analysis, if heterogeneity of variances was observed. Data are presented as means ± SE. When variables are depicted in figures or evaluated by statistics, the comparisons are always performed between similar groups (similar n values). Data are presented as means over 1.5-, 3-, and 6-h periods, respectively.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Cardiovascular responses.
MAP increased slightly during Supine and Prone from 88 ± 2 to
92 ± 2 mmHg (Table 1). The same
pattern was observed for SAP and DAP, in that SAP increased at the end
of the intervention period from 117 ± 2 to 122 ± 2 mmHg
during Supine and from 118 ± 2 to 122 ± 2 mmHg during Prone
and DAP increased from 73 ± 1 to 77 ± 2 mmHg and from
73 ± 2 to 77 ± 1 mmHg, respectively. PP varied
insignificantly between 44 ± 1 and 47 ± 3 mmHg during
Supine and Prone. HR increased slightly during Prone from 54 ± 2 to 58 ± 2 beats/min and varied insignificantly during Supine
(Fig. 1). No significant changes occurred
in left atrial diameter during Supine and Prone.
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1 · l1 (Fig. 1).
During Supine, there were no significant changes in stroke volume or
total peripheral vascular resistance.
Plasma osmolality. Plasma osmolality decreased during Supine from 284 ± 1 to 281 ± 1 mosmol/kgH2O (P < 0.05; Table 1), whereas no significant changes were observed in Prone.
Endocrine responses.
Plasma concentration of NE increased during Prone from a mean value of
the preintervention period of 97 ± 9 to a maximum of 123 ± 16 pg/ml (P < 0.05; Table 1). There were no
significant changes during Supine, where NE varied insignificantly
between 90 ± 13 and 108 ± 15 pg/ml. E was increased by
Prone from 12 ± 2 to a maximum of 21 ± 3 pg/ml
(P < 0.05), whereas no significant changes occurred in
Supine. Plasma concentration of aldosterone varied insignificantly
between 34 ± 4 and 55 ± 6 pg/ml and that of plasma
vasopressin varied insignificantly between 1.5 ± 0.2 and 3.1 ± 0.9 pg/ml. During Supine, plasma ANP decreased from 64 ± 10 to
a nadir of 41 ± 7 pg/ml and PRA increased from 550 ± 140 to
850 ± 200 pg · ml1 · h1
(P < 0.05; Table 1). ANP increased during the initial
measurement of Prone (P < 0.05; Table 1). In Prone,
there was a numeric increase in PRA solely due to an increase in one
subject to 4,500 pg · ml1 · h1 at the 9th h
but no significant changes due to a decrease in another subject (Table
1).
Renal responses.
UNaV increased similarly during Supine and Prone over time
to peak values during the 6th h. Mean values over 3-h periods are depicted in Table 2. The cumulated
UNaV during the 6 h of intervention was 69 ± 3 mmol/6 h for Supine and 76 ± 5 mmol/6 h for Prone. UosmV exhibited a temporal profile very similar to that of
UNaV (Table 2). At the beginning of the experiment,
Uosm was high (up to 670 ± 50 mosmol/kgH2O) due to overnight dehydration. Thereafter, it
varied insignificantly between 157 ± 16 and 298 ± 43 mosmol/kgH2O. UKV exhibited a very similar
pattern during Supine and Prone, respectively, with a decrease over
time (P < 0.05; Table 2).
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Additional study.
During Lateral, there was a decrease in MAP from 90 ± 2 to a mean
value of 85 ± 2 mmHg and a simultaneous increase in left atrial
diameter from 32 ± 1 to 35 ± 1 mm (P < 0.05; Table 3). HR varied insignificantly
between 54 ± 3 and 56 ± 4 beats/min (Table 3). There were
no significant changes in plasma osmolality or in NE (Table 3), and
renal variables did not differ significantly from those of Supine. Thus
cumulated V over the 6 h of Lateral was 1,352 ± 64 ml/6 h,
cumulated CH2O was 349 ± 41 ml/6 h, and cumulated
UNaV was 68 ± 5 mmol/6 h. The 24-h renal sodium
excretion following the standardized sodium intake was 115 ± 11 mmol/24 h and thus very similar to that of Supine.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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The results demonstrate that changing the direction of the transverse G-stress (±1 Gx and +1 Gy) in humans had only little or no effects on renal variables. The prone position slightly increased CH2O and V but had no statistically significant effect on renal sodium handling. During Prone, however, there was a decreased stroke volume and increased sympathetic nervous activity as indicated by the increase in HR, total peripheral vascular resistance, and plasma concentration of NE. The left lateral position did not affect the renal variables but increased left atrial diameter and decreased arterial pressures. Thus compression of the thorax in Prone might have caused the 16% decrease in stroke volume, whereby a slightly attenuated pulsation of the arterial tree might have inhibited baroreflexes leading to an increase in sympathetic nervous activity. It is noteworthy, however, that this seemed to have no effect on renal sodium and water handling, but it is possible that the antinatriuretic effect was opposed by the simultaneous increase in ANP. The decrease in MAP in Lateral could have been caused by left atrial distension leading to a low-pressure baroreflex-mediated peripheral vasodilatation.
Surprisingly, results of recent studies performed by us indicated that the natriuresis of a saline infusion in space was lower than that of ground-based simulation of microgravity by head-down bed rest (2, 6, 22). Furthermore, plasma NE was unexpectedly high in space (21, 22). Fritsch-Yelle et al. (10) showed that arterial pressures are consistently decreased in space compared with during ambulatory ground-based conditions. Therefore, because the acute supine or 6° head-down position on the ground does not accurately reflect the effects of microgravity on renal fluid and sodium handling in humans, we hypothesized that the transverse gravitational component from front to back (±1 Gx) or from side to side (±1 Gy) modulates cardiovascular and renal variables.
Previous results from parabolic flights demonstrated that left atrial diameter increases and MAP decreases during transition from 1 to 0 g in supine humans, whereas no changes occur when the subjects are placed in the left lateral position (25). This suggests that the transverse G-stress affects arterial pressures and cardiac filling and that 1 Gx and 1 Gy modulate cardiovascular reflexes. In this study, we therefore also investigated the effects of changing position from supine to left lateral.
Effects of prone. It is a theoretical possibility that compression of the thorax in Prone accounted for the slight but significant decrease in stroke volume. This decrease in stroke volume may reflect a decrease in arterial filling and pulsation leading to some inhibition of the arterial baroreceptors. This could, in turn, have caused the increase in sympathetic nervous activity, HR, and total peripheral vascular resistance.
Plasma ANP was increased after 1.5 h of Prone, which could have been caused by the increase in HR (13), as it is unlikely that cardiac filling was increased, because stroke volume decreased and left atrial diameter was unaffected. It is possible that the effect of increased plasma ANP counteracted the antinatriuretic effect of the increased sympathetic nervous activity with subsequent minimal changes in renal sodium output. The similar increases in FENa during Supine and Prone suggest that the tubular handling of sodium did not differ between the postures. A mechanism for the small diuresis and increase in CH2O in Prone cannot readily be explained from the data we collected, because we did not observe significant changes in plasma concentration of vasopressin or in GFR. Because, however, the diuresis was only in the magnitude of 150 ml over the 6 h and the increase in CH2O of some 100 ml compared with during Supine, these small changes are probably biologically insignificant. Thus Prone decreases stroke volume and increases sympathetic nervous activity, HR, and total peripheral vascular resistance, and to only a small degree it increases CH2O and V. The slight increases in renal outputs are not readily explicable from our data.Effects of lateral. When the subjects were placed on their left lateral side, we observed an increase in left atrial diameter and a simultaneous decrease in MAP. These results are in accordance with previous observations from our laboratory (25). The mechanisms of the hypotensive effects of Lateral probably involve stimulation of cardiopulmonary low-pressure reflexes, as indicated by the increased left atrial diameter obtained by a decrease in intrathoracic pressure (9) or by facilitated venous return due to less compression of the inferior caval vein by the intra-abdominal organs. Changes in the shape of the thorax and abdomen (32) could, through a decrease in intrathoracic pressure per se, also have contributed to the decrease in MAP (14). Thus the decrease in MAP during Lateral was probably due to the combined effects of peripheral vasodilatation induced by cardiopulmonary low-pressure receptor stimulation and the mechanical effects of a decrease in intrathoracic pressure. The small decrease in MAP should, however, be interpreted with caution, because it is very difficult to determine the exact hydrostatic reference point for arterial pressure measurements. An error of a few millimeters Hg can therefore not be excluded. Because HR was unchanged in Lateral, the decrease in MAP must have been caused by peripheral vasodilatation, which is supported by the decrease in DAP.
Plasma osmolality was not changed by Prone and Lateral but was decreased by Supine. Usually, the present hydration regime decreases Posm during supine conditions (23). It is, however, surprising that Posm did not decrease in Prone and Lateral. The increase in CH2O in Prone can only partially explain that Posm was above that of Supine. Another explanation could be that absorption of water from the gastrointestinal tract was reduced by Prone and Lateral or that evaporation from the skin was increased. All of these suggestions, however, are purely speculative and need further investigation. In conclusion, the hypothesis that changing the direction of the transverse G-stress in horizontal humans modulates cardiovascular and renal variables was partly confirmed. Prone reduced stroke volume and increased sympathetic nervous activity, HR, and total peripheral vascular resistance. This effect may have been caused by some compression of the thorax leading to impediment of arterial filling and thus inhibition of arterial baroreflexes. There was no statistically significant effect on renal sodium handling. The slightly but probably biologically insignificant increase in CH2O in Prone cannot be explained from the present results. Furthermore, Lateral induced an increase in left atrial diameter and a simultaneous decrease in MAP. We suggest that facilitated venous return in Lateral caused stimulation of the low-pressure receptors, which again together with decreased intrathoracic pressure caused the hypotensive effects.Perspectives
The cardiovascular and renal changes observed in the present study are small, and the mechanisms behind them are unclear. It is, however, not unlikely that these effects, although small, could have an impact in regard to patients who are confined to bed for long periods. Especially in patients with cardiac or fluid volume regulatory disorders, it is possible that the present observed effects could be enhanced over time. It should be noted that the prone position enhances sympathetic nervous activity in normal subjects. Such an increase would probably be inappropriate for, e.g., heart patients, in which baseline levels of plasma NE are already elevated. It is, however, unknown if plasma NE increases further, if heart patients are placed in the prone position. In contrast, the left lateral posture might be beneficial for some heart patients, because venous return is facilitated and MAP is reduced. Therefore, further investigations of the effects of horizontal posture changes could be of importance for defining the best-suited posture for patients during hospitalization.| |
ACKNOWLEDGEMENTS |
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The technical assistance of L. Soot, M. Gybel, E. Larsen, and J. Oxbøl is gratefully acknowledged.
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FOOTNOTES |
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This study was supported by Grant #3.12.03-25/95, ESA-FF-1/96 and 9602455 from the Danish Research Councils.
Address for reprint requests and other correspondence: B. Pump, Dept. of Aviation Medicine, The Heart Centre, Rigshospitalet 7522, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
First published February 28, 2002;10.1152/ajpregu.00619.2001
Received 11 October 2001; accepted in final form 26 February 2002.
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TOP
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RESULTS
DISCUSSION
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) or
prone position (Prone; 
). Values are means ± SE
of 6 healthy males. #Mean value of the 6-h intervention period
significantly differed from that of the initial 3 h of supine
preintervention, P < 0.05. (#)Significant difference
by least significant difference test. bpm, Beats/min.