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1 Neurology Division, St. Marianna University School of Medicine, Kawasaki, Kanagawa 216-8511, Japan; 2 Department of Aviation Medicine, National University Hospital, DK-2100 Copenhagen, and 3 Department of Internal Medicine and Endocrinology, Herlev University Hospital, 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 acute water immersion to the neck (WI) compared with 6° head-down tilt (HDT) induces a more pronounced distension of the heart and lower plasma levels of vasoconstrictor hormones. Ten healthy males underwent 30 min of HDT, WI, and a seated control (randomized). During WI, left atrial diameter and stroke volume increased to the same extent as during HDT. Cardiac output increased by 1 l/min more during WI than during HDT. (P < 0.05). Plasma atrial natriuretic peptide increased during WI (P < 0.05) but not during HDT, whereas plasma norepinephrine, vasopressin, and renin activity were suppressed similarly. Mean arterial pressure decreased by 9 mmHg (P < 0.05) during HDT and was unchanged during WI, and heart rate decreased more during HDT (P < 0.05). Arterial pulse pressure increased considerably more during HDT than during WI. In conclusion, the hypothesis was not confirmed because the cardiac atria were similarly distended by acute HDT and WI and the release of vasoconstrictor hormones were suppressed to the same extent.
weightlessness; pressures; neurohormones
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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DURING THE PAST DECADES, 6° head-down tilt (HDT) and water immersion to the neck (WI) have been utilized to simulate the cardiovascular effects of weightlessness in humans (4, 6, 8, 15, 18). During both of these interventions, blood and fluid are redistributed from the caudal to the cephalic portions of the body, leading to an increased venous return. This increase in venous return induces distension of the heart and adjacent vessels, which leads to stimulation of volume and pressure receptors. Simultaneously, the release of atrial natriuretic peptide (ANP) is increased and the plasma levels of vasopressin, norepinephrine, renin, and aldosterone are decreased through neuronal pathways (4, 6, 15, 18).
Although WI and HDT have been used to simulate the effects of weightlessness, recent results from space indicate that neuroendocrine and renal responses to weightlessness are not in compliance with those of prolonged HDT (16, 17). Renal responses to saline or water loading in space are attenuated compared with those on the ground, and sympathetic nervous activity is higher. Therefore, it is doubtful whether HDT correctly simulates the effects of weightlessness. WI could be a more suitable model. To define the best-suited ground-based model to simulate the effects of weightlessness, the first step is to compare the cardiovascular and neuroendocrine effects of the two models. The next step could then be to compare the effects of the two models with those of spaceflight.
Previous results from our laboratories have indicated that WI induces a higher increase in central venous pressure with a more pronounced natriuresis than HDT (15). Therefore, we tested the hypothesis that the heart is more distended during WI than during HDT with a higher cardiac output (CO), stroke volume (SV), and plasma ANP level and lower plasma concentrations of vasoconstrictor hormones.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Ten healthy men (age = 28 ± 1 yr; height = 180 ± 2 cm; weight = 75 ± 2 kg) participated in the experiment. All had a negative history of cardiovascular and kidney disease and were healthy as indicated by a normal physical examination, arterial pressure (<140/90 mmHg), electrocardiogram, and urine strip tests for glucose, leukocytes, erythrocytes, and proteins. None of the subjects took any medication for at least 1 mo before the study. Informed consent was obtained after subjects had read a description of the experimental protocol, which was approved by the Ethics Committee of Copenhagen (KF 01-323/96) and was in compliance with the Declaration of Helsinki. No complications occurred.
Subjects arrived at the laboratory at 8:00 AM on the day of study and were weighed. A short catheter (Venflon2, internal diameter = 1.2 mm; length = 45 mm) was inserted into a cubital vein for blood sampling, and the subject thereafter rested in the seated position for at least 30 min. The protocol consisted of three parts with the sequence randomized in a balanced fashion among subjects and performed consecutively on the same day. Each part lasted 90 min and consisted of 30 min of a seated baseline followed by 30 min of either WI, HDT, or a seated control, which again was followed by 30 min of a seated recovery. Measurements were performed from minutes 15-25 during each 30-min interval in the following sequence: echocardiography for left atrial diameter (LAD) determination, blood sampling and measurements of arterial pressures, heart rate (HR), and CO. Room temperature was kept between 23.3 and 26.5°C, humidity between 28 and 51%, and water temperature between 34.5 and 34.8°C.
WI was performed by using an electrical hoist to lower a chair suspended from the ceiling with subjects seated into an insulated plastic tank filled with tap water. Posture change from upright seated to 6° HDT was performed by passively tilting a back support to 6° head down. When seated, subjects sat upright in a chair with body axis and lower legs vertical, thighs horizontal, and feet resting on a support.
LAD was measured by echocardiography (Aloka SSD 500, Silmonsen and Weel) according to the criteria of Feigenbaum (5). During end expiration, 3M-Mode pictures (printouts from a recorder, Sony SVO-9500 MDP) were obtained from the parasternal long-axis view. From these, LAD was subsequently determined.
Blood samples were collected from the cubital vein and immediately
transferred into chilled tubes. Samples were placed on ice and
subsequently centrifuged at 3,700 rpm at 4°C for 10 min. The plasma
was then frozen and stored at 
25°C for later determinations of
plasma concentrations of vasopressin, catecholamines, ANP, and plasma
renin activity (PRA). After each sampling, the amount of collected
blood was substituted with the same amount of isotonic saline. Plasma
vasopressin and ANP were measured by a radioimmunoassay as previously
described (12, 23), whereas catecholamines were measured
by a radioenzymatic assay (13). PRA was measured by an
antibody-trapping method (20). Plasma osmolality and
plasma protein concentration were measured in triplicate on fresh
samples by freezing-point depression (Advanced Instruments; 3MO Plus) and refractometry (Belliagham and Stauley), respectively.
Systolic (SAP) and diastolic arterial pressure (DAP) were measured in the right brachial artery by conventional sphygmomanometry and auscultation. The first and fourth Korotkoff sounds were used for detection of SAP and DAP, respectively. Arterial pulse pressure (PP) was calculated from SAP minus DAP and MAP from adding one-third of PP to DAP. In addition, peripheral mean arterial pressure (MAPp) in the finger and HR were measured by a photoplethysmographic method (2300 Finapress, Ohmeda) in the left index finger.
CO was measured by a rebreathing method with an infrared photoacoustic multigas analyzer (AMIS 2001, Innovision A/S, Odense, Denmark) as previously described in detail (3). A gas mixture of 1% SF6, 5% N2O, and 50% O2 in N2 with a gas volume of 30% of the calculated vital capacity was used (2). Total peripheral vascular resistance (TPR) and SV were calculated from MAPp/CO and CO/HR, respectively, and MAPp and HR were recorded during rebreathing.
Data are presented as means ± SE. An ANOVA (Statgraphics plus for Windows, version 3.0) 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 interventions (WI, HDT, and control, respectively). 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, HDT, and control, respectively) and subjects as factors. Differences between mean values were evaluated by a post hoc multiple-range test (Newman-Keuls) or a paired t-test. A significance level of 0.05 was chosen.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Cardiovascular responses.
LAD increased during WI from 27 ± 1 to 34 ± 1 mm and
similarly during HDT from 26 ± 1 to 33 ± 2 mm
(P < 0.05, Fig. 1). CO increased during HDT from 4.6 ± 0.3 to 5.4 ± 0.3 l/min
(P < 0.05, Fig. 1) with a further increase
(P < 0.05) during WI from 4.2 ± 0.3 to 6.4 ± 0.3 l/min (P < 0.05, Fig. 1). HR decreased during WI from 70 ± 2 to 64 ± 2 beats/min (P < 0.05) with a more pronounced decrease during HDT from 68 ± 2 to
57 ± 2 beats/min (P < 0.05, Fig.
2). SV increased from 58 ± 4 to
94 ± 4 ml during WI (P < 0.05, Fig. 1) and
similarly from 65 ± 4 to 88 ± 4 ml during HDT (P < 0.05, Fig. 1) with no change during seated
control.
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Neuroendocrine responses.
Plasma concentration of ANP increased during WI from 28 ± 5 to
44 ± 6 ng/ml (P < 0.05) and was unchanged during
HDT (Fig. 3). Plasma NE, AVP, and PRA
decreased similarly during WI and HDT with no changes during seated
control (Fig. 3).
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Plasma composition. Plasma osmolality did not change during any of the procedures. Plasma protein decreased from 70 ± 1 to 66 ± 1 during WI (P < 0.05) and very similarly during HDT from 70 ± 1 to 67 ± 1 (P < 0.05, Table 1).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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The results of this study indicate that the cardiac atriae are similarly distended by HDT and WI, and release of vasoconstrictor hormones are suppressed to the same extent. Therefore, the hypothesis was not confirmed. Furthermore, arterial baroreflexes must have been stimulated to a higher degree during HDT than during WI, because the carotid baroreceptors were statically stimulated by the posture change, per se, and PP was higher. This static stimulation of the carotid baroreceptors and pulsatile stimulation of all of the arterial baroreceptors led to lower MAP at heart level and lower HR compared with during WI. The more pronounced increase in CO and plasma ANP during WI than during HDT might have been caused by the lesser decrease in HR.
Cardiac distension and ANP release. Plasma ANP increased during WI and was unchanged during HDT (Fig. 3). This indicates that the cardiac atria were more distended during WI. LAD, however, was similar. Therefore, we suggest that the higher HR during WI than during HDT induced a higher CO and ANP release (10). Because we also observed a lower TPR during WI (Fig. 2), it is possible that this difference was caused by the difference in plasma ANP, because ANP possesses vasodilatory capabilities (1).
In a previous review (15), our laboratory reported that central venous pressure increased more during WI than during HDT. Because the transmural distension pressure was not measured, we in fact do not know whether the heart is more distended during WI. The very similar increase in LAD during the two interventions indicates that distension pressure increases to a similar extent. Alternatively, it is also conceivable that cardiac compliance differs, comparing effects of WI with those of HDT. These issues can only be clarified by measuring central venous pressure and esophageal pressure simultaneously (7). This will shed light on whether the more pronounced increase in plasma ANP during WI than during HDT is caused by atrial distension or a higher HR.Baroreflexes and blood pressure control. Arterial baroreceptors were stimulated by WI because PP increased significantly. Furthermore, cardiopulmonary, low-pressure receptors must also have been stimulated because LAD and ANP release increased. Thus two sets of pressure receptors, arterial high and cardiopulmonary low, probably potentiated the effects of each other (21, 22). During HDT, both sets of receptors were also stimulated, but to different degrees than during WI, because arterial pulsation was more pronounced and carotid baroreceptors were hydrostatically stimulated by the posture change per se. Effects of hydrostatic stimulation of carotid baroreceptors and higher PP are reflected in lower MAP at heart level and lower HR than during WI. The lower MAP in the aorta during HDT must have inhibited the aortic baroreceptors and thus buffered the hypotensive effects of stimulation of the carotid receptors. In this way, a new equilibrium was obtained with a 9-mmHg-lower MAP during HDT.
The 9 ± 2 mmHg-lower MAP during HDT than during WI is in compliance with previous results from our laboratory (19) and those of others (9). One would, however, have expected that MAP and HR during a posture change from seated to HDT would return to the level of the seated control due to the buffering effects of inhibition of the aortic baroreceptors. This is in fact the case during static neck suction. Pump and colleagues (21, 22) have shown that the simultaneous increase in central blood volume with distension of the heart and the increase in PP during a posture change from seated to supine probably account for the maintained lower MAP and HR. Because TPR decreased more during WI than during HDT, this cannot explain the lower MAP during HDT. Therefore, the more pronounced decrease in HR during HDT, which caused less of an increase in CO than during WI, is probably the reason for the decrease in MAP. The lack of increase in MAP during WI despite the pronounced increase in CO must primarily have been accomplished by peripheral vasodilation (11), which is indicated by the decrease in TPR. This vasodilation must, therefore, mainly have been induced by stimulation of cardiopulmonary low-pressure reflexes, possibly in combination with some stimulation of arterial baroreceptors, as indicated by the moderate increase in PP. Comparing the effects of WI and HDT on TPR and HR (Fig. 2) might lead to the notion that peripheral vasodilation during an antiorthostatic maneuver is induced primarily by cardiopulmonary low-pressure stimulation, whereas HR is governed more by arterial baroreceptors.Vasoactive hormones. Suppression of vasoconstrictor hormone releases was very similar when comparing the effects of WI and HDT. This indicates that cardiac distension is responsible for the neuroendocrine changes through stimulation of cardiopulmonary low-pressure receptors. Had the interventions been longer than 30 min, another picture might have emerged because our laboratory has previously observed that, during graded WI, more than 30 min are required to induce small but detecable differences in renin release (14). Therefore, we are cautious to declare that only cardiac distension caused the changes in release of vasoconstrictor hormones (18).
In conclusion, the results of this study indicate that the cardiac atria are similarly distended by acute HDT and WI and that the release of vasoconstrictor hormones are similarly suppressed. Therefore, the hypothesis that WI causes greater atrial distension than HDT was not confirmed. Furthermore, carotid baroreflexes are stimulated to a higher degree during HDT than during WI due to abolishment of the hydrostatic gradient from head to heart, and arterial baroreflexes are more stimulated by a more pronounced elevation in PP. This leads to lower HR during HDT, which may explain that plasma ANP is lower than during WI, because atrial distension was similar comparing the effects of the two conditions.| |
ACKNOWLEDGEMENTS |
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We gratefully acknowledge the assistance of Anders Gabrielsen, Bettina Pump, Maria Gefke, and Tsutomu Kamo.
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FOOTNOTES |
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This study was supported by Grant 9802910 from the Danish Research Councils.
Makoto Shiraishi was a guest scientist at the Danish Aerospace Medical Centre of Research during the course of the study.
Address for reprint requests and other correspondence: M. Shiraishi, Neurology Division, St. Marianna University School of Medicine, 2-16-1, Sugao, Miyamae-ku, Kawasaki-shi, Kanagawa-ken 216-8511, Japan (E-mail: shira{at}marianna-u.ac.jp).
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.
Received 29 December 2000; accepted in final form 5 September 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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), water immersion (WI; 
), and
6° head-down tilt (HDT; 
). Each intervention is
preceded and followed by 30 min of being seated. Values are means ± SE of n = 10 (CO, SV) or n = 9 (LAD). *Significant difference between WI and HDT at same points in
time (P < 0.05). #Significant difference
compared with values of initial 30 min in the seated position
(P < 0.05).
