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1 Section of Cardiology, To test the
hypothesis that head-down-tilt bed rest (HDBR) for 14 days alters
vascular reactivity to vasodilatory and vasoconstrictor stimuli, the
reactive hyperemic forearm blood flow (RHBF, measured by venous
occlusion plethysmography) and mean arterial pressure (MAP, measured by
Finapres) responses after 10 min of circulatory arrest were measured in
a control trial (n = 20) and when
sympathetic discharge was increased by a cold pressor test (RHBF + cold
pressor test; n = 10). Vascular
conductance (VC) was calculated (VC = RHBF/MAP). In the control trial,
peak RHBF at 5 s after circulatory arrest (34.1 ± 2.5 vs.
48.9 ± 4.3 ml · 100 ml
forearm blood flow; vascular conductance; muscle sympathetic nerve
activity; reactive hyperemia
VASCULAR TONE is a determinant of blood flow and blood
pressure regulation during physiological maneuvers such as exercise and
upright posture. Interestingly, spaceflight and its ground-based analog
head-down-tilt bed rest (HDBR) reduce exercise capacity and orthostatic
tolerance. These observations suggest that blood vessel regulation may
be altered by spaceflight and bed rest.
Evidence for impaired vasodilatory function after bed rest can be
inferred from the classic experiments of Saltin et al. (26), who
observed augmented arteriovenous oxygen differences at a given oxygen
uptake during submaximal cycling exercise after bed rest. The cardiac
output response to submaximal exercise was not reduced. These data
suggest that peripheral vasodilation was reduced after bed rest. Also,
slowed kinetics of the increase in oxygen uptake during the transition
from rest to cycling exercise have been observed after bed rest (8). In
addition, Overton et al. (23) observed augmented iliac artery vascular
resistance and reduced leg blood flow during submaximal exercise
performed by rats after head-down suspension. Together, these data
suggest that the vasodilatory response to metabolic stimuli is
attenuated by spaceflight and bed rest.
It has also been suggested that vasoconstrictor responses are impaired
after head-down immobilization. For example, several investigators,
using the head-down suspension model in rats, have shown that this
analog of spaceflight leads to diminished reactivity of vascular tissue
to constrictor stimuli (11, 22, 36). In humans, however, arterial
infusion studies have suggested that the constrictor responses are
unchanged after bed rest (5). The reasons for these different
observations are unclear.
The purpose of this study was to investigate the effect of HDBR on
vasodilatory capacity and on the ability of an increase in sympathetic
discharge to constrict a dilated vascular bed. We measured the reactive
hyperemic forearm blood flow (RHBF) response after 10 min of
circulatory arrest to investigate the hypothesis that bed rest reduces
the ability to dilate peripheral vascular tissue. To assess the effect
of bed rest on vascular sensitivity to sympathoexcitation, the RHBF
response was measured in the absence and presence of a cold pressor
test. The tests were performed before and after 14 days of
Subjects
ABSTRACT
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Abstract
Introduction
Methods
Results
Discussion
References
1 · min1)
and VC (0.34 ± 0.02 vs. 0.53 ± 0.05 ml · 100 ml1 · min1 · mmHg1)
were reduced in the post- compared with the pre-HDBR tests
(P < 0.05). Total excess RHBF over 3 min was diminished in the post- compared with the pre-HDBR trial (84.8 vs. 117 ml/100 ml, P < 0.002). The
ability of the cold pressor test to lower forearm blood flow was less
in the post- than in the pre-HDBR test
(P < 0.05), despite similar
increases in MAP. These data suggest that regulation of vascular
dilation and the interaction between dilatory and constrictor
influences were altered with bed rest.
INTRODUCTION
Top
Abstract
Introduction
Methods
Results
Discussion
References
6° HDBR. The results show that RHBF was reduced by the
bed-rest period, suggesting a reduced dilatory capacity. Also, the
ability to constrict a dilated bed during a cold pressor test (CPT) was
attenuated.
METHODS
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Abstract
Introduction
Methods
Results
Discussion
References
HDBR
During HDBR the average daily caloric intake for the subjects was ~2,500 kcal, which consisted of ~55% carbohydrate, 25% fat, and 20% protein. Daily dietary sodium was ~3,000 mg. Fluids were allowed ad libitum, but the subjects were encouraged to consume
2,000 ml/day.
Each day the photoperiod was 16 h of light, with lights on at 0700. Vital signs of blood pressure, heart rate (HR), and tympanic
temperature were assessed four times daily at 4-h intervals while the
subjects were awake. Body weight was assessed every other day.
Experimental Design
RHBF (n = 20). RHBF was measured on 2 separate days. The first test was performed ~2 wk before the bed-rest period began. The second test was performed on day 14 of the HDBR. In the laboratory each subject assumed the supine position, and the midforearm was positioned 10 cm above the heart. The subjects were then instrumented for forearm blood flow (FBF), HR (electrocardiogram), and blood pressure (Finapres, Ohmeda, Madison, WI) measurements. FBF was measured using venous occlusion plethysmography with a single-strand mercury-in-rubber strain gauge (18). Pneumatic cuffs were placed around the upper arm and the wrist of the right arm. The strain gauge was positioned around the forearm at the point of the greatest forearm circumference. Care was taken to position the strain gauge in the same location in the pre- and post-HDBR tests. Blood flow was measured by first inflating the wrist cuff to 250 mmHg to exclude hand blood flow from the FBF measurements (21), then briefly inflating the upper arm occlusion cuff to 50 mmHg. The Finapres pneumatic finger blood pressure cuff was placed on the hand of the left arm, which was positioned level with the heart.
Baseline FBF measurement, which commenced after 1 min of wrist occlusion (21), was determined as the average of 8-10 repeated measurements over 3-5 min. After these measurements, FBF was measured after 10 min of forearm circulatory arrest. Circulatory arrest for 10 min is a potent peripheral vasodilator stimulus and achieves repeatable levels of peak RHBF (29). The initial blood flow was measured at 5 s after release of circulatory arrest, with subsequent measurements at 15 s after cuff release and every 15 s thereafter for a total collection period of 3 min. In our hands, these methods have provided repeatable measurements of RHBF and vascular conductance (VC) on different days (31).RHBF + CPT (n = 10).
Ten of the above subjects performed a second RHBF protocol 15 min
after the previous bout of forearm ischemia. The purpose of the
second RHBF test was to determine the effect of prolonged HDBR on the
ability to vasoconstrict a maximally dilated vascular bed by elevating
sympathetic discharge by use of the CPT. The CPT is a potent
nonspecific sympathoexcitatory stimulant (37). The CPT was initiated
after 9 min of forearm ischemia by placing a foot in ice water.
The RHBF measurements then commenced at 10 min of forearm circulatory
arrest (i.e., after 1 min of CPT). The pressor response to ice
application is maximal between 1 and 2 min (37). Therefore, we reasoned
that the RHBF during the first 60 s after release of circulatory
arrrest would provide the best indication of HDBR effects
on the ability to constrict a dilated bed. Because the CPT is a potent
sympathetic stimulus that likely increases epinephrine release, we were
concerned about the possible prolonged effects of this test on
neurohumoral function. Therefore, the CPT maneuver always followed the
control trial.
Data Analysis
The effect of HDBR and time during each test on RHBF, MAP, and HR after 10 min of ischemia was assessed by repeated-measures two-way ANOVA by using the Statistical Analysis System (SAS, SAS Institute, Cary, NC) with planned comparisons focused on the measurements obtained at 5, 15, 30, 45, and 60 s after circulatory arrest. Bonferroni's correction was used to maintain P at <0.05 in the multiple comparisons.The effect of CPT on RHBF was assessed in two ways. First, a repeated-measures three-way ANOVA was used to assess the effect of HDBR, CPT, and time on FBF, MAP, HR, and VC after the ischemia. This allowed us to determine whether CPT-induced vasoconstriction occurred in the pre- and post-HDBR tests. To assess whether the effect of CPT was different between the pre- and post-HDBR trials, we calculated the difference in FBF, VC, MAP, and HR between the control and CPT trials for each of the pre- and post-HDBR tests. These differences were compared using a two-way ANOVA to test for the effect of bed rest and time. For the analysis of the effects of CPT, planned comparisons were made at 5, 15, 30, 45, and 60 s after cuff release by using Bonferroni's correction of the probability level.
Differences in TEF with HDBR were assessed using Student's two-tailed paired t-test. For all comparisons the level of significance was P < 0.05. Values are means ± SE.
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RESULTS |
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Methods
Results
Discussion
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Baseline Measurements
Baseline HR increased from 65 ± 2 beats/min in the pre-HDBR tests to 71 ± 2 beats/min in the post-HDBR tests (P < 0.005). FBF at rest was not different between post- and pre-HDBR (3.10 ± 0.3 and 3.28 ±0.5 ml · 100 ml1 · min1,
respectively). Baseline MAP was not different in the pre- and post-HDBR
tests (90.4 ± 2.0 and 95.1 ± 2.0 mmHg, respectively). Also,
baseline VC was not different in the pre- and post-HDBR tests (0.04 ± 0.0 and 0.03 ± 0.0 ml · 100 ml1 · min1 · mmHg1,
respectively).
RHBF
HR and MAP were greater during the 3-min period after release of circulatory arrest in the post- than in the pre-HDBR tests (main effect, P < 0.0001; Fig. 1). The absence of condition-by-time interactions suggests that the greater postischemia HR and MAP were related, at least in part, to elevated baseline values. The bed-rest period resulted in a reduction in the FBF response after 10 min of circulatory arrest (main effect, P < 0.0001). On the basis of planned comparisons, the RHBF levels at 5, 45, and 60 s after circulatory arrest were significantly reduced in the post- compared with the pre-HDBR tests (Fig. 2; P < 0.0001). Because of the combined reductions in RHBF and the increased MAP, VC was reduced in the post- compared with the pre-HDBR tests (main effect, P < 0.0001; Fig. 2). With the exception of 15 s, VC in the first 60 s after the release of the cuff was significantly reduced after bed rest. TEF was also reduced in the post- compared with the pre-HDBR tests (Fig. 3; P < 0.005).
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CPT
Immersion of the foot in ice water significantly raised HR and MAP in the pre- and post-HDBR tests (P < 0.0001). Before the bed-rest period, the CPT resulted in a significant reduction in RHBF (main effect, P < 0.05; Fig. 4). Also, forearm VC was reduced with CPT (main effect, P < 0.05), with statistically significant pointwise differences at 15, 45, and 60 s after cuff release (Fig. 4). In the post-HDBR tests the small reductions in FBF with the CPT did not reach statistical significance; however, VC was diminished (main effect, P < 0.05; Fig. 4). Compared with the pre-HDBR condition the absolute FBF and VC values during the CPT were not different during the first 45 s of the RHBF period in the post-HDBR test. However, FBF and VC with the CPT were significantly reduced in the post-HDBR test after 1 min of RHBF measurements (P < 0.05; not shown on Fig. 4). This difference at 1 min postischemia is difficult to interpret, because the corresponding FBF values measured in the pre-HDBR test with ice were similar to those measured in the post-HDBR test without ice.
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To assess the effect of bed rest on the ability of the CPT to increase
HR and MAP and to reduce RHBF and VC, the change in these variables
(
HR, MAP, FBF, and VC) evoked by immersion of the foot in
the ice bath was calculated. The increase in MAP during the first 60 s
after release of circulatory arrest was not different in the pre- and
post-HDBR trials. In contrast, HR increased more with CPT in the post-
than in the pre-HDBR condition (P < 0.01; Fig. 5), with planned comparison
pointwise differences at 30 and 45 s after release of circulatory
arrest. At 5 s after cuff release, RHBF was reduced during RHBF + CPT
in the pre-HDBR trial by 4.78 ± 3.9 ml · 100 ml1 · min1
but was increased in the post-HDBR trial by 7.96 ± 3.9 ml · 100 ml1 · min1
(P < 0.0001; Fig.
6). For the 1st min of reactive hyperemia, the ability of the CPT to reduce RHBF and VC was less in the post- than
in the pre-HDBR trial (main effect, P < 0.001).
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DISCUSSION |
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The first major finding of the present study was that the peak FBF and VC at 5 s after 10 min of circulatory arrest and the TEF during the RHBF protocol were attenuated after 14 days of HDBR. These data suggest that the ability of the forearm vasculature to dilate in response to ischemia was impaired by bed rest. A second observation was that the ability of the CPT to vasoconstrict the forearm during the RHBF maneuver was attenuated by bed rest.
It is likely that the peak response (i.e., the FBF measured at 5 s after cuff release) is an indication of vasodilation that occurred during the period of circulatory arrest. The causes of dilation during circulatory arrest may include myogenic reductions in arterial tone, metabolite accumulation, and prostaglandin production (4, 24, 35). In addition, the number of microvascular units available for dilation may contribute to the peak RHBF. After this initial peak response, regulation of the time course of recovery appears to include nitric oxide (14, 20, 33) and possibly histamine (12), with little contribution from metabolite levels (2). Thus comparisons of peak and total postischemic flow are important indexes to follow in order to understand the effects of bed rest on forearm vasodilation. In our report, both responses were attenuated, suggesting that HDBR impairs multiple vascular dilatory systems.
The mechanism of the reduced peak and total RHBF after bed rest cannot be determined from the current data. In contrast to leg muscles, 2 wk of bed rest do not appear to alter forearm strength (17) and, by inference, total muscle mass. However, it is not known how the deconditioning effects of bed rest affect metabolic regulation and autoregulation of vascular tone during forearm circulatory arrest.
In view of the observations of diminished dilation during the control
trials, we tested a second hypothesis that 14 days of HDBR would alter
the interplay between competing dilator and constrictor factors. To
test this hypothesis, the RHBF response was measured when sympathetic
discharge was elevated by a CPT. In previous experiments it was shown
that a CPT could reduce forearm conductance after ischemia by a
sympathetically mediated, rather than a myogenic, mechanism (32). Also,
preliminary data from seven subjects in our laboratory suggest that
between 60 and 90 s of the CPT the ability to augment muscle
sympathetic activity is not different between pre- (276 ± 162 %
units) and post-HDBR tests (306 ± 81 % units,
P > 0.2) (unpublished data).
Therefore, the CPT is useful for examination of the neurovascular
responsiveness to sympathetically mediated constriction.
In these studies, forearm vasodilation was reduced after bed rest. Therefore, we cannot exclude the possibility that the attenuated vasoconstrictor response after bed rest was due, at least in part, to the lower level of postischemic blood flow after bed rest. Additionally, if CPT responses are directly compared before and after bed rest, we find that VC and FBF during the first 45 s of RHBF measurements were not statistically different, whereas VC and FBF were lower at the 60-s measurement after bed rest. This analytic approach would suggest that vasoconstrictor responses were unchanged after bed rest. However, on the basis of VC and FBF data, shown in Figs. 4-6, we believe the most appropriate assessment is that elevated sympathetic discharge retained the ability to constrict a maximally dilated vascular bed after HDBR but the magnitude of this effect was diminished. For example, at 5 s after circulatory arrest in the post-HDBR test, the CPT evoked an increase in FBF (not a decrease) above the no-ice trial (Fig. 6) at a time when the CPT-induced increase in MAP was not different from the pre-HDBR condition (Fig. 5).
The interpretation of diminished constrictor responses to sympathoexcitation is consistent with recent evidence of diminished sympathetic nervous system activity in some subjects after bed rest (16, 27) and that some subjects exhibit an attenuated ability to vasoconstrict during a stand test after spaceflight (3, 15). Also, investigators have used a head-down suspension model in rats to demonstrate an impaired ability to reduce limb blood flow with increased sympathetic activation (22) and a reduced ability for isolated aortic strips to generate tension for a given level of suffusate norepinephrine (10, 11). This evidence of diminished constrictor responses also discounts the possibility that enhanced vasoconstriction occurred during circulatory arrest and RHBF after bed rest, a response that might simultaneously account for the diminished vasodilation and constriction responses. Further arguments against the idea of enhanced baseline constrictor tone come from evidence that forearm circulatory arrest by itself does not evoke sympathoexcitation (30) and baseline forearm vascular resistance is reduced (1) or unchanged (7, 28) with bed rest.
The reduced vasoconstrictor response after HDBR raises the question,
How was MAP maintained during the CPT at pre-HDBR levels? The answer
may lie in the HR responses. HR and MAP were increased with CPT in both
tests. However, after bed rest the same increase in MAP was
accomplished with greater increases in HR. Perhaps the elevated HR
resulted in a greater cardiac output to maintain the increase in MAP in
the presence of diminished peripheral constriction.
The present results suggest that simultaneous reductions in dilatory
and constrictor responses in forearm muscle vascular tissue develop
during prolonged bed rest. Thus complex and profound alterations in
vascular control are exhibited, likely involving multiple regulatory
mechanisms. A unifying hypothesis that might explain the altered
control of HR and reduced peripheral vascular constrictor responses
with bed rest may be an upregulation of 
-adrenergic receptors
subsequent to diminished norepinephrine release that develops during
prolonged bed rest (25). Enhanced vascular -adrenergic
responsiveness after bed rest has been observed (9). With this
adaptation, an increase in sympathetic discharge, such as would occur
with a CPT, would have an augmented dilatory effect in resistance
vessels and an increased chronotropic effect on HR. As a result,
systemic blood pressure would be maintained by an augmented HR and
cardiac output and perfusion of peripheral muscle beds would be
protected. These counterbalancing adaptations may also explain why the
increase in HR on standing is greater after spaceflight and bed rest
(3, 15, 34), despite diminished parasympathetic nervous system control
of HR (13, 19). These adaptations cannot explain the diminished
dilation after ischemia.
The reduced dilator and constrictor responses observed after bed rest may explain in part the reduced aerobic capacity and orthostatic intolerance seen after HDBR. Peak aerobic capacity is governed by a complex interaction of cardiorespiratory and vascular factors. In addition to reduced maximal cardiac output, plasma volume, and oxygen-carrying capacity (see Ref. 6 for review), a reduced ability to vasodilate could reduce the magnitude and alter the distribution of flow within a given muscle. In addition, many individuals completing prolonged periods of spaceflight and/or bed rest experience an intolerance for orthostasis, possibly because of an attenuated ability to constrict the peripheral vasculature (3). Thus the diminished constrictor responses observed in the present study may have important ramifications for the maintenance of blood pressure on going from the supine to the upright position after prolonged convalescence or spaceflight.
In summary, the present data indicate that the peak vasodilatory response to ischemia is attenuated after 14 days of HDBR. In addition, the ability to constrict a dilated vascular bed was diminished after bed rest, but the magnitude of this latter response is difficult to assess because the forearms did not dilate as much. Nonetheless, these data are the first to indicate that, in humans, vascular reactivity to competing dilatory and constrictor stimuli may be altered by bed rest.
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ACKNOWLEDGEMENTS |
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We appreciate the nursing care provided by the staff of the Pennsylvania State General Clinical Research Center at The Milton S. Hershey Medical Center. We thank A. Kunselman for statistical advice.
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FOOTNOTES |
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This work was supported by National Aeronautics and Space Administration Grant NAGW-4400 (L. I. Sinoway), National Institutes of Health (NIH) Grant R01 AG-12227 (L. I. Sinoway), a Department of Veterans Affairs Merit Review Award (L. I. Sinoway), and NIH General Clinical Research Center with Division of Research Resources Grant M01 RR-10732. J. K. Shoemaker was supported by a Natural Sciences and Engineering Research Council of Canada postdoctoral fellowship. D. H. Silber was the recipient of an NIH National Research Service Award.
Address for reprint requests: J. K. Shoemaker, Sect. of Cardiology, The Milton S. Hershey Medical Center, The Pennsylvania State University College of Medicine, MC H047, PO Box 850, Hershey, PA 17033.
Received 24 November 1997; accepted in final form 22 January 1998.
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