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Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, N-0317 Oslo, Norway
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The hypothesis tested was that there are significant
transient changes in the cardiovascular variables after rapid onset and release of mild lower body negative pressure (LBNP, 
20 mmHg), even in
experimental situations where there is no detectable change in
steady-state values. Twelve subjects participated in the study. Heart
rate, stroke volume (SV), cardiac output, mean arterial pressure (MAP),
total peripheral resistance (TPR), acral and nonacral skin blood flow,
and blood flow velocity in the brachial artery were continuously
recorded during the pre-LBNP period (0-120 s), during LBNP
(120-420 s), and during the post-LBNP period (420-600 s). The
main finding was that MAP is transiently but strongly affected by rapid
changes in LBNP as small as 20 mmHg. There was also a characteristic
asymmetry in cardiovascular responses to the onset and release of LBNP,
particularly in the responses in SV. The transient changes in MAP
indicate that the neural responses that affect TPR are not fast enough
to compensate for the rapid changes in LBNP. In this case, the arterial
baroreceptors will be activated as well as the low-pressure
baroreceptors that sense central venous pressure. This must be taken
into consideration in future discussions of the results of LBNP protocols.
lower body negative pressure; cardiovascular control; mean arterial pressure; stroke volume
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THE LOWER BODY NEGATIVE
PRESSURE (LBNP) technique was introduced by Stevens and Lamb
(20) in 1965 to study circulatory responses to simulated
gravitational shifts of blood in humans. LBNP induces fluid shifts by
pooling blood in the legs and abdomen and activates a number of
cardiovascular adjustments that tend to maintain central blood volume
and arterial pressure. The cardiovascular responses to different levels
and durations of LBNP have been widely studied during the last 40 years
(1, 2, 6, 7, 15, 20), and the steady-state responses to
different levels of LBNP are well known. Although different techniques
have been used to measure the cardiovascular variables and to apply
LBNP, there is relatively good agreement between the steady-state
results in comparable studies. It is generally agreed that there is a
decrease in central venous pressure (CVP), stroke volume (SV), cardiac
output (CO), and forearm and leg blood flow, and an increase in total
peripheral resistance (TPR) and heart rate (HR) on the introduction of
LBNP. It is also generally accepted that mean arterial pressure (MAP) is not affected by mild LBNP (0 to 20 mmHg) (15).
During lower levels of LBNP (0 to 20 mmHg), most authors report no
change in MAP (6, 13, 14, 16); however, others have
reported a small increase (12) or decrease in MAP
(9, 17).
Because mild LBNP has traditionally been expected not to affect MAP, it
has frequently been used to study the influence of cardiopulmonary
baroreceptors on the human circulatory system. Some studies have
questioned the concept that arterial pressure is maintained perfectly
during mild hypovolemia by reflexes triggered by cardiopulmonary
receptors (17, 21). Taylor et al. (21) used
nuclear magnetic resonance imaging to measure the dimensions of a major
barosensory area, the thoracic aorta, during different levels of LBNP.
They were able to detect significant decreases in the ascending aortic
pulse area during LBNP as mild as 10 mmHg. These authors found no
significant changes in arterial pressure during 10 mmHg LBNP with
uncontrolled breathing, but they showed that during controlled
breathing, 10 mmHg LBNP increased systolic and pulse pressure.
Pannier et al. (17) studied the pulsatile changes in blood
pressure and arterial diameter with applanation tonometry and
echo-tracking techniques at the sites of the common carotid artery and
the carotid arterial bulb during 10 and 40 mmHg LBNP. They reported
cyclic changes in tension for even 10 mmHg LBNP. Those studies show
that the arterial baroreceptors are probably affected during the
"steady-state" period of mild LBNP as well, even though changes in
MAP are not normally detected.
A common feature of all studies using the LBNP technique to study circulatory responses to simulated gravitational shifts of blood in humans is that cardiovascular responses have not been continuously measured but only sampled once or a few times at different levels of LBNP.
Thus, despite of the large numbers of studies where the LBNP technique has been used to study cardiovascular responses to gravitational shifts of blood, the time course of these cardiovascular responses has not yet been studied systematically. This is probably because of a lack of methods to measure beat-to-beat SV noninvasively or because it has not been possible to control the LBNP chamber with sufficient accuracy at the onset and release of LBNP. Regardless of the reason, knowledge of the transient cardiovascular responses caused by gravitational shifts of blood is still poor.
We expected that there might be significant transient changes in the cardiovascular variables that are different from those found during the steady-state periods of mild LBNP. We assumed such changes have not been detected in previous studies, because the time resolution of recordings of the cardiovascular variables has been too low or because they have been smoothed out because data have been averaged over specific time periods. If such transient changes occur during the onset and release of LBNP, they may contribute to the precise regulation of MAP reported during mild LBNP.
Our group previously developed and improved an ultrasound Doppler technique for continuous recording of beat-to-beat SV for long periods of time (5). To be able to study the transient cardiovascular responses caused by rapid shifts of blood, we developed and constructed an LBNP chamber that allows us to regulate precisely both the rate of pressure change and the set LBNP level. We can thus record the cardiovascular variables with a high sample frequency and regulate the onset, release, and extent of LBNP very precisely.
Our hypothesis is that there are significant transient changes in the
cardiovascular variables after rapid onset and release of mild LBNP
(20 mmHg) even in experimental situations where there is no
detectable change in steady-state values.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects. Twelve volunteers, six female and six male {age 23.3 (2.9) yr [mean (SD)], height 175.5 (6.0) cm, weight 67.7 (9.2) kg}, were studied. All were nonsmokers and in good physical shape. None was taking any medication. The subjects were not allowed to drink coffee or tea on the experimental day or to exercise or eat for at least 2 h before the start of the experiment. Written informed consent was obtained from all participants, and the study was approved by the local ethics committee.
Experimental design. The experiments were carried out at the University of Oslo. Each test subject was lightly clothed and lay comfortably on a bench, with the lower body inside the LBNP chamber, which was sealed at the level of the iliac crest. The ambient temperature was between 25 and 28°C and was adjusted to obtain large fluctuations in the brachial arterial blood flow velocity, indicating that the subjects were in their thermoneutral zone (22). The subjects were acclimatized for 30 min before the experiment started. The experiment started with a 2-min period at room pressure in the LBNP chamber. This period is defined as the pre-LBNP period. Two minutes after recording started, the pressure in the LBNP chamber was rapidly lowered to 20 mmHg below room pressure. This period lasted 5 min and is defined as the LBNP period. Five minutes after the onset of LBNP, the pressure in the LBNP chamber was released and returned to room pressure. This period lasted 3 min and is defined as the post-LBNP period. Five identical experiments were run for each test subject, two on the first visit to the lab and three on the second visit. All experiments were carried out between 9 AM and 4 PM, and each test subject was asked to arrive at the lab to start the experiment at the same time for both visits to reduce any effects of his or her circadian rhythm.
LBNP.
LBNP was applied using a custom-built chamber and pressure-control
system designed to introduce rapid changes in LBNP. The chamber is a
transparent polymethylmethacrylate (PMMA) tube that encloses the
patient's lower body. This tube is connected to a vacuum pump
and tank via hoses and motor-actuated valves. Pressure inside the
chamber is monitored by a pressure sensor (Lucas Novasensor NPC-1210).
A microcontroller compares the measured pressure with the pressure set
point at a frequency of 50 Hz. If there is a difference, the controller
sends signals to the valves to modulate chamber pressure and reduce the
difference. In this study, the pressure was reduced to 20 mmHg below
room pressure in <0.3 s and then returned to room pressure in <0.3 s.
Figure 1 shows the pressure in the LBNP
chamber during one experiment.
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Measurements. Beat-to-beat SV was recorded by an ultrasound Doppler method (5). A bidirectional ultrasound Doppler velocimeter (SD-100, GE Vingmed Ultrasound, Horten, Norway) was operated in pulsed mode at 2 MHz with a hand-held transducer. The ultrasound beam was directed from the suprasternal notch toward the aortic root, and the sample volume range was adjusted so that measurements were made 1-2 cm above the aortic valve. We positioned the sample volume range centrally in the aorta by searching for the highest obtainable velocity signal. An angle of 20° between the direction of the sound beam and the bloodstream was assumed in the calculations. To remove vessel wall and valve motion artifacts, together with any recorded diastolic movement of blood, the built-in high-pass filter in the SD-100 was set to remove signals originating from velocities of <0.275 m/s. The output of the SD-100 maximum velocity estimator and a three-lead surface electrocardiogram (ECG) were interfaced online to a personal computer. In a separate session, the diameter of the rigid aortic ring was determined by parasternal sector scanner imaging (CFM-750, GE Vingmed Ultrasound). We assumed that the orifice was circular and used this diameter to calculate the area of the aortic valvular orifice. SV was calculated by multiplying the value obtained by numerical integration of the recorded instantaneous maximum velocity during each R-R interval by the area of the orifice. This calculation is based on the assumption that the velocity profile is rectangular at the level of the valves and that this velocity is conserved as the central maximum velocity of a jet 3-4 cm upward in the aortic root (4, 5). Instantaneous HR was obtained from the duration of each R-R interval of the ECG signal. Beat-to-beat CO was calculated from the corresponding HR and SV values. Blood flow velocity in the brachial artery was measured using the ultrasound Doppler technique (SD-50, GE Vingmed Ultrasound). The operating frequency was 10 MHz. The circular transducer had a fixed angle of 45° between the sound beam and the underlying skin surface. The transducer was fastened to the skin of the cubital fossa with adhesive tape, and the ultrasound beam was directed toward the brachial artery. The instantaneous cross-sectional mean velocity was calculated by the SD-50 and fed online to the computer for beat-by-beat time averaging, gated by the ECG R waves. Laser-Doppler technique (MBF3D, Moore Instruments, Devon, UK) was used to measure skin blood flow in the pulp of the left second finger (acral skin area) and in the skin of the forearm (nonacral skin area). The laser-Doppler probes were fastened to the skin with narrow double-sided tape (Kontron Instruments). The noise-limiting filter of the instrument was set at its highest level (21 kHz), and the emitted wavelength was 820 nm. The flux output signal was filtered with a time constant of 0.1 s and sent to the computer. The sampling frequency was 2 Hz. Finger arterial pressure was recorded continuously (2300 Finapress BP, monitor, Ohmeda, Madison, WI). Care was taken to adjust the arm so the finger was at heart level. The instantaneous pressure output was transferred online to the recording computer, and beat-to-beat MAP was calculated by numerical integration. Arterial pressure obtained by this method has been shown to be in good accordance with central intra-arterial pressure in various situations (11, 18). TPR was calculated as MAP divided by CO (mmHg min/l). MAP was used as an approximation to the perfusion pressure across the systemic circulation, assuming CVP to be zero and unchanged by LBNP. CO was used as an estimate for averaged flow through the resistance vessels. We did not measure CVP in this study and are aware that we have probably overestimated TPR during LBNP, because venous pressure is lower in this period than before and after LBNP.
Data analysis. SV and blood flow velocity in the brachial artery were sampled beat by beat, gated by the ECG R waves. CO, MAP, and TPR were calculated for every heart beat. Acral and nonacral skin blood flow were sampled at a frequency of 2 Hz. Before the data were analyzed, all recorded variables were converted into a 2-Hz sampled signal by interpolation. Throughout the registration period, there is considerable beat-to-beat variation in the recorded variables. This variation has been reported by other authors (5, 8) and is partly due to the influence of respiration (8, 23). Variations in the recorded variables not related to the onset and release of LBNP were partly eliminated by calculating the average response from five identical experiments run in each subject. This was done using the coherent averaging technique (19, 24) synchronized by the onset of LBNP. Finally, we pooled the individual average curves for the twelve subjects for calculation of the interindividual averaged responses by finding the mean value in each set of synchronous samples for each 2-Hz time step (24). Frey et al. (6) studied women's responses to different levels of LBNP in the follicular and luteal phases of the menstrual cycle. They concluded that there were no significant differences between these two phases in the responses to LBNP. Frey et al. (6) also concluded that the responses of the women in their study to LBNP were qualitatively similar to those reported for male subjects (24). We have therefore considered the results from the females and males together in the present study. The mean value for the steady-state part of the pre-LBNP period (0-120 s) for each cardiovascular variable was used as a reference value. In a first statistical analysis, this value was compared with the value for the same variable in the steady-state part of the LBNP period (180-420 s) and the value in the steady-state part of the post-LBNP period (480-600 s). ANOVA for repeated measures was used to test for significant differences. If there was a significant difference, the values were tested against each other. Bonferroni adjustment of the P value for multiple comparisons was used. In a second analysis, transient values of the variables, observed a specified time after the onset and release of LBNP, were added to the model and were tested in the same way as previously described. All the analyses were performed using the statistical program SPSS. Differences were considered significant at P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Mean SV, HR, CO, MAP, TPR, acral skin blood flow, and blood flow
velocity in the brachial artery from the whole registration period (600 s) are shown at left of Fig.
2. Changes in the same variables in the
10 s before to 60 s after the onset (A) and the release (B)
of LBNP are shown at right.
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Steady-state levels.
All the physiological variables showed relatively stable resting values
in the pre-LBNP period (0-120 s). All the measured variables also
showed stable values after the first 60 s of the LBNP period
(180-420 s) and the post-LBNP period (480-600 s). Table
1 shows the mean values for SV, HR, CO,
MAP, TPR, acral and nonacral skin blood flow, and blood flow velocity
in the brachial artery in the pre-LBNP period (0-120 s), the
steady-state part of the LBNP period (180-420 s), and the
steady-state part of the post-LBNP period (480-600 s).
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Onset of LBNP.
There were dramatic changes in the measured variables shortly after the
onset of LBNP. Approximately 8 s after the onset of LBNP, SV
started to decrease. During the next 50 s, it gradually dropped
about 18% (slope 0.3 ml/s) and then stabilized at this level during
LBNP. There was a small transient increase in HR in the first seconds
after the onset of LBNP, followed by a slow rise in the next 60 s,
before HR stabilized. Because the changes in HR were relatively small,
CO showed a very similar pattern to SV the first part of the LBNP
period. CO stabilized after about 60 s at a level about 15% lower
than in the control period (slope 8.7 ml/s).
Release of LBNP.
There were also dramatic changes in the physiological variables after
the release of LBNP. After ~1 s we observed a significant transient
drop in SV (P = 0.008). In the following 8 s, SV
rose rapidly to about the same level as before LBNP (slope 2.62 ml/s). SV returned to pre-LBNP level during about 10-12 s after release of LBNP, whereas it took ~60 s before SV stabilized after onset of
LBNP. There was a further slight increase in SV in the next 2 min. HR
increased immediately after the release of LBNP and then dropped in the
next 3 s before increasing again to a maximum level about 17 s after the release of LBNP. Figure 3
clearly shows the negative correlation between HR and SV in the first
6 s after the release of LBNP. We observed a drop in CO (9%)
corresponding to the drop in SV ~1 s after the release of LBNP.
Because the changes in SV were larger than those in HR, CO was still
closely correlated with SV immediately after the release of LBNP. MAP rose significantly ~16% immediately after the release of LBNP (P < 0.0005). After ~5 s, it started to fall,
reaching a minimum level significantly (~22%) under the mean level
in the steady-state part of the LBNP period (P = 0.002). It then rose again and after ~21 s stabilized at the same
level as before LBNP and in the steady-state part of the LBNP period.
During the first 2 s after the release of LBNP, TPR rose
significantly (P < 0.0005), to ~15% above the mean
level in the steady-state part of the LBNP period. It then dropped
gradually in the next 12 s to significantly (~26%) below the
mean level in the steady-state part of the LBNP period
(P = 0.002). After this it increased again and
stabilized at the same level as before LBNP, ~25-30 s after the
release of LBNP. We did not observe any significant changes in nonacral
skin blood flow after the release of LBNP. Acral skin blood flow was
also unchanged for the first 3 s after the release of LBNP, but
after this we observed a significant decrease (P = 0.049). The time course and magnitude of this reduction in acral skin
blood flow were very similar to what we observed immediately after the
onset of LBNP. In the subsequent 10 s, acral skin blood flow
increased again to about the same level as before LBNP. Blood flow
velocity in the brachial artery increased in the first 3 s after
the release of LBNP. A drop corresponding to the drop in acral skin
blood flow followed this. Blood flow velocity in the brachial artery then increased steadily and stabilized at about the same level as
before LBNP.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Cardiovascular changes at the onset and release of LBNP. Using our improved LBNP chamber, we observed cardiovascular changes at the onset and release of LBNP that to the best of our knowledge have not previously been described in the literature.
The most important finding in this study was that MAP is transiently but strongly affected by rapid changes in LBNP, even those as small as20 mmHg. Because mild LBNP has traditionally been expected not to
affect MAP, mild LBNP has frequently been used to study the influence
of cardiopulmonary baroreceptors on the human circulatory system. Our
findings, however, suggest that the neural responses that affect TPR
are not fast enough to compensate for rapid changes in LBNP. In this
case, the arterial baroreceptors will be activated in addition to the
low-pressure baroreceptors that sense CVP, even for mild LBNP. Figure 3
shows the relationship between MAP and HR in the pre-LBNP period and
during the onset of LBNP and the first part of the LBNP period. The
transient changes in HR corresponding to the transient changes in MAP
during the onset of LBNP clearly indicate a baroreflex involvement.
Taylor et al. (21) and Pannier et al. (17)
have also both challenged the concept, and they provided results that
indicated that the arterial baroreceptors are probably affected during
steady state of mild LBNP, even though changes in MAP are not normally detected. These findings must be taken into consideration in future discussions of the results of LBNP protocols where the aim is to elicit
reflex responses mediated by cardiopulmonary baroreceptors without
activating the arterial baroreceptors.
After the rapid onset of LBNP we also observed a delay of ~8 s before
SV started to fall. During this period, SV in the left ventricle is
probably maintained by depleting the blood "stored" in the
pulmonary vessels (26). Hoffman et al. (10)
showed that when a dog was suddenly held upright for 20-30 s,
right ventricular SV fell immediately, but the fall in left ventricular
SV was delayed by 6-8 heartbeats. We did not measure CVP or right
ventricle SV, but we believe that it is reasonable to expect the same
pattern in our subjects after the onset of LBNP.
Eight seconds after the rapid onset of 20 mmHg LBNP, a steady
decrease in SV started. SV stabilized at a level ~19% lower than the
pre-LBNP level about 50 s after the onset of LBNP. After the
release of LBNP, however, SV rose to its pre-LBNP value in ~10 s.
Toska and Walløe (25) also described this asymmetry in the SV response in a study in which they recorded beat-to-beat SV in
healthy humans during passive head-up tilt to 30°. They found that SV
took 30 s to adjust on head-up tilt but stabilized at its pretilt
value during the first 10 s after tilt back to a supine position.
We believe that the asymmetry in the SV response after rapid changes in
body position or LBNP can be explained mainly mechanically. After the
onset of LBNP, the venous valves will restrict backward filling of the
veins in the lower body. These veins must therefore be filled
exclusively from the arterial side, in spite of the rapid reduction in
LBNP. After the end of LBNP, the pressure around the veins suddenly
increases, and the blood stored in the expanded veins during LBNP will
rapidly be returned to the central circulation. This will cause an
immediate increase in CVP and may result in a rapid adjustment of SV
back to pre-LBNP values. Even if the CVP starts to decrease immediately after onset of LBNP, it appears to take 50 s before SV reaches a
stable level.
Immediately after the release of LBNP, we also observed a transient
fall in SV, the lowest values being reached ~2-2.5 s after the
release of LBNP. SV was then ~12% below the stable level at the end
of LBNP and 28% lower than before LBNP. In the following 8 s, SV
returned to about the same level as before LBNP. The large drop in SV
immediately after the release of LBNP is probably explained by many
factors, one of which may be interventricular interaction. The sudden
increase in filling of the right side of the heart may cause a
reduction in the volume of the left side and thus a lower left
ventricular SV. In addition, there may be an "afterload effect,"
i.e., a rise in end systolic volume resulting from the sudden increase
in MAP. We observed a considerable increase in MAP immediately after
the release of LBNP.
Figure 4 shows the relationship among
MAP, SV, and HR after the release of LBNP. HR increased the first few
seconds, but reached its peak level later than SV reached its lowest
value. The increase in HR is caused by reduced vagal activity. It is
well known that the vagal response time is shorter than the sympathetic
response time. During the period of stable LBNP, we expect the
myocardial contractile force to be set at a stable level. The
sympathetic response affecting myocardial contractile force is not fast
enough to compensate for the sudden increase in MAP, and, as a result, the end systolic volume increases and SV decreases.
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Steady-state values during LBNP.
In the present study, we obtained steady-state values during LBNP
corresponding to a 19% reduction in SV, a 7% rise in HR, a 15%
reduction in CO, no change in MAP or nonacral skin blood flow, a 24%
reduction in acral skin blood flow, and a 25% reduction in blood flow
velocity in the brachial artery. At the end of the post-LBNP period,
the variables started to stabilize at around the same values as
before. These findings are in accordance with those
previously described for the steady-state periods before, during, and
after exposure to 20 mmHg LBNP.
Perspectives
Despite the large numbers of studies where the LBNP technique has been used to study cardiovascular responses to gravitational shifts of blood, the continuous time course of the cardiovascular variables has not yet been studied systematically. Therefore, knowledge of the transient cardiovascular responses caused by gravitational shifts of blood is still poor. In this study, we have revealed that there are significant transient changes in SV, HR, CO, TPR, acral skin blood flow, blood flow velocity in the brachial artery, and, most importantly, in MAP. Mild LBNP has traditionally been considered to elicit reflex responses mediated by cardiopulmonary baroreceptors only, without any arterial baroreflex involvement. However, because there are clear transient effects on MAP, at least during rapid onset and release of mild LBNP, it is possible that the arterial baroreceptors are in fact activated. If this is the case, they will contribute to the precise regulation of MAP reported during mild LBNP. This may be a potential artifact that must be taken into consideration in drawing conclusions from LBNP studies. In the future, care should be taken to observe transient changes in MAP during the onset and release of LBNP.| |
ACKNOWLEDGEMENTS |
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The authors thank the 12 volunteers for participation in this study. We also thank Professor Emeritus B. A. Waaler for valuable discussions and A. Sira, Ø. Løkeberg, and E. Salberg for technical assistance with the design and construction of the LBNP chamber.
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FOOTNOTES |
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This work was supported by the Norwegian Council on Cardiovascular Diseases.
Preliminary results from this study were presented as a poster at Experimental Biology, Washington, DC, 1999.
Address for reprint requests and other correspondence: J. Hisdal, Dept. of Physiology, Inst. of Basic Medical Sciences, Univ. of Oslo, PO Box 1103 Blindern, N-0317 Oslo, Norway.
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 November 1999; accepted in final form 7 March 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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