(Circulation. 1995;91:1725-1731.)
© 1995 American Heart Association, Inc.
Articles |
Effect of Continuous Positive Airway Pressure on Intrathoracic and Left Ventricular Transmural Pressures in Patients With Congestive Heart Failure
From the Divisions of Respirology (M.T.N., T.D.B.) and Cardiology (M.A.R., K.H., J.S.F.) and the Centre for Cardiovascular Research, Department of Medicine of the Toronto Hospital, University of Toronto, Toronto, Ontario, Canada.
Correspondence to T. Douglas Bradley, MD, 212-10EN Toronto Hospital (TGD), 200 Elizabeth St, Toronto, Ontario, Canada M5G 2C4.
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Abstract |
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Background Continuous positive airway pressure (CPAP) can improve cardiac function in patients with congestive heart failure (CHF). We hypothesized that this effect might be related to CPAP-induced increases in intrathoracic pressure, which would reduce left ventricular transmural pressure (LVPtm) during systole, thereby decreasing left ventricular afterload.
Methods and Results The effect of graduated CPAP from 0 to 10 cm H2O on the above variables was examined over a 75-minute period and compared with a 75-minute time control period without CPAP in two groups of subjects: 15 patients with CHF and 9 healthy subjects. Intrathoracic pressure was estimated from esophageal pressure (Pes), and systolic LVPtm, a determinant of left ventricular afterload, was assessed by subtracting Pes during systole from systolic blood pressure. Cardiac index (CI) was assessed by Doppler echocardiography. At baseline, inspiratory Pes amplitude, which reflects inspiratory muscle force generation, was greater in the patients with CHF than in the healthy group (9.9±0.8 versus 5.5±0.4 mm Hg, P<.001). In addition, systolic Pes, which represents the relative contribution of intrathoracic pressure to LVPtm, was more negative in the patients with CHF than in the healthy group (-4.1±0.3 versus -2.2±0.1 mm Hg, P<.001). While on CPAP of 10 cm H2O, inspiratory Pes amplitude decreased and systolic Pes increased significantly in the group with CHF (from 11.1±1.1 to 7.5±1.1 mm Hg, P<.025 and from -4.7±0.6 to 0.6±0.6 mm Hg, P<.001, respectively), but CPAP had no effect on these variables in the healthy subjects. Compared with the equivalent time control period, Pes amplitudexrespiratory rate decreased significantly while on CPAP in both the group with CHF (from 188±22 to 112±17 mm Hgxbreaths per minute, P<.005) and the healthy group (from 82±8 to 60±6 mm Hgxbreaths per minute, P<.05). Compared with time control, systolic LVPtm decreased significantly while on CPAP, from 116.0±5.3 to 110.3±4.5 mm Hg (P<.025) in the group with CHF, but did not change in the healthy group. Moreover, systolic LVPtmxheart rate decreased significantly in the group with CHF (from 80.55±5.27 to 71.83±4.73 mm Hgxbeats per minute/100, P<.005) but not in the healthy group. CI decreased significantly while on CPAP in the healthy group (P<.025) but did not change in the group with CHF.
Conclusions In patients with CHF, the inspiratory muscles generate greater force per breath and systolic Pes contributes more to LVPtm than in healthy subjects. By increasing intrathoracic pressure in patients with CHF, CPAP unloaded inspiratory muscles and reduced left ventricular afterload without compromising CI.
Key Words: ventricles • pressure • heart failure
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Introduction |
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Continuous positive airway pressure (CPAP) administered via a face or nasal mask can acutely augment cardiac output in patients with poorly compensated congestive heart failure (CHF).1 2 Chronic improvements in left ventricular ejection fraction (LVEF) have also been reported with nightly application of CPAP in patients with CHF and coexistent obstructive or central sleep apnea.3 4 5 It has been postulated that CPAP exerts its effects on cardiac performance by increasing intrathoracic pressure and thereby reducing cardiac preload, by impeding cardiac filling, and afterload, by reducing left ventricular transmural pressure (LVPtm).1 2 6 7 Reductions in preload and afterload in response to CPAP have been documented in experimental animals with healthy cardiac function as demonstrated by decreases in left ventricular end-diastolic and end-systolic volumes.7 8 9 There also is evidence that CPAP can reduce heart rate in patients with CHF.2 10 However, the effect of CPAP on intrathoracic pressure and left ventricular afterload in humans with CHF has not been determined.
Vasodilators exert their beneficial effects on cardiac function in CHF primarily by reducing left ventricular afterload secondary to reducing vascular resistance.11 12 If CPAP also reduces left ventricular afterload in patients with chronic CHF, this effect might contribute to improved cardiac function.1 2 3 4 We hypothesized that because CPAP raises intrathoracic pressure, it should reduce LVPtm during systole (the difference between left ventricular systolic pressure and extracardiac pressure)6 and thereby reduce left ventricular systolic wall stress. If CPAP simultaneously reduces heart rate in patients with CHF, it should reduce pressurexheart rate, an important determinant of myocardial O2 consumption.10 13 Therefore, the objectives of the present study were to determine the effects of CPAP on intrathoracic pressure, LVPtm, and LVPtmxheart rate in patients with CHF and in healthy subjects.
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Methods |
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Subjects
Volunteers free of cardiac or respiratory disease were recruited as healthy subjects. Patients less than 75 years of age with chronic CHF were recruited on the basis of a history of CHF secondary to ischemic or idiopathic dilated cardiomyopathy for at least 6 months, chronic exertional dyspnea despite medical therapy, and a left ventricular ejection fraction <45% measured by 99Tc equilibrium radionuclide angiography. The protocol was approved by the Ethics Committee for Human Experimentation at the University of Toronto, and all subjects gave consent before entering the study.
Arterial and Esophageal Pressures
Blood pressure was measured
every minute with an automatic
sphygmomanometer (PhysioControl Lifestat 200). Heart rate was derived
from a precordial ECG lead. Esophageal pressure (Pes) was
measured using a balloon catheter system attached to a pressure
transducer (45±50 cm H2O, Validyne MP) placed in the
esophagus according to the method of Baydur et al14 such
that change in Pes equaled change in mouth pressure during
occluded breaths. Respiratory movements were detected by a pneumobelt
from which respiratory rate was calculated. ECG,
Pes, and pneumobelt output were recorded
continuously onto a strip-chart recorder (model 2800S, Gould).
Stroke Volume and Cardiac Output
Stroke volume and cardiac
output were determined by Doppler
echocardiography (Ultramark 8, Advanced Technology Laboratories) as
previously described for our laboratory.15 With patients
in the supine position, maximum instantaneous aortic flow velocity was
measured in the ascending aorta using continuous wave Doppler (2.25
MHz) directed through the suprasternal window. Stroke volume was
calculated from the product of the mean time-velocity integral and the
cross-sectional area of the aortic annulus orifice (A):
A=
(D/2)2, where D is the diameter of the aortic
annulus obtained from a prior parasternal long-axis view at baseline.
In addition, in four healthy subjects and four patients with CHF,
aortic annular diameter was determined during the application of 10 cm
H2O of CPAP. Aortic annular diameter did not change from
baseline to CPAP of 10 cm H2O in either the healthy
subjects (from 2.04±0.06 to 2.04±0.05 cm) or the patients with
CHF
(from 1.71±0.08 to 1.72±0.08 cm). We therefore assumed no change
in
aortic annular area in those receiving CPAP. Integrals for 30 to 60
heartbeats were averaged to obtain a mean time-velocity integral that,
by taking into account inspiratory and expiratory phases, would
represent an average over the entire respiratory cycle. Cardiac
output was calculated from the product of stroke volume and heart rate.
Stroke volume index (SVI) and cardiac index (CI) were then derived
taking into account the body surface area.
Protocol
Healthy subjects and patients with CHF were studied
during a
time control period and while receiving CPAP (BiPAP, Respironics Inc)
for a 75-minute period, while awake and supine on two consecutive
afternoons in random order. Thus, both healthy subjects and patients
with CHF acted as their own controls. On the time control day, after a
15-minute baseline recording period without a mask on, an open mask
with a 3-cm lumen of negligible resistance was placed over each
subject's nose with the mouth closed for 45 minutes and then was
removed for 15 minutes. On the CPAP day, after a 15-minute baseline
period, CPAP was applied via a tightly fitting nasal mask with the
mouth closed for 15 minutes at each of three consecutive pressures—5,
7.5, and 10 cm H2O (3.7, 5.5, and 7.4 mm Hg,
respectively)—followed by a 15-minute recovery period without
CPAP.
Statistical Analysis
End-expiratory Pes during the
initial recording
period on each of the 2 days was considered the baseline
value.16 The average end-expiratory
Pes, amplitude of end-expiratory Pes to
peak inspiratory Pes, peak inspiratory
Pes compared with baseline end-expiratory
Pes, and Pes during cardiac systole
measured synchronously with the QRS complex of the ECG were calculated
from the last 2 minutes of each 15-minute interval. Although maximum
left ventricular systolic pressure is generated between the QRS and T
waves, the QRS is a more distinct reference point for systole and
provides a convenient method of determining an appropriate sampling
frequency for the determination of systolic LVPtm and
systolic LVPtmxheart rate. This sampling method also takes
into account the exposure of the left ventricle to Pes
during both inspiration and expiration to give an average systolic
Pes throughout the respiratory cycle (Fig 1
). Since
brachial artery systolic pressure accurately
reflects left ventricular end-systolic pressure in the absence of
aortic outflow obstruction, LVPtm values at the peak of
inspiration and during cardiac systole were calculated by subtracting
peak inspiratory Pes and systolic Pes (ie, the
most negative and mean Pes values to which the heart is
exposed during systole), respectively, from the average brachial
systolic blood pressure during each time interval. Systolic
LVPtmxheart rate was used as another index of afterload
that adjusts for changes in heart rate.10 13 The
Pes amplitudexrespiratory rate product was used as an
index of inspiratory muscle force generation and energy requirement
over time.17 18
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Comparisons between data for the healthy group and for the group with CHF at baseline were made using two-tailed unpaired t tests. Two-way ANOVA for repeated measures was used to compare variables on the CPAP day with the equivalent time control period within both the healthy and CHF groups. For the purposes of clarity, P values reported in the text refer to comparisons at 10 cm H2O of CPAP and the equivalent time control period unless otherwise stated. A value of P<.05 was considered statistically significant. Results are expressed as mean±SEM.
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Results |
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Subject Characteristics
Nine healthy subjects and 15 patients with CHF were studied. Ten patients had ischemic and 5 had idiopathic dilated cardiomyopathy. One CHF patient was female but in all respects responded to CPAP in a fashion similar to the male patients. Twelve patients were in sinus rhythm and 3 were in atrial fibrillation. Left ventricular ejection fraction in the group with CHF was reduced at 17.9±2.4%. The patients with CHF were normoxic and eucapnic (PaO2 of 82.3±3.1 mm Hg and PaCO2 of 39.8±2.2 mm Hg). Vasodilators were being taken by all patients, digoxin by 66%, and diuretics by 93%.
The characteristics of the subjects are shown in the
Table. The groups were comparable for body mass index
and baseline respiratory rates. Pes amplitude, peak
inspiratory Pes (which, at baseline, is identical to
Pes amplitude), and Pes amplitudexrespiratory
rate were significantly greater (P<.001), whereas systolic
Pes was significantly more negative in the group with CHF
than in the healthy group (P<.001). The healthy group and
the group with CHF mean heart rates and diastolic blood pressures were
comparable. However, as one would expect, the group with CHF had a
lower systolic blood pressure, SVI, and CI (P<.001)
compared with the healthy group. Although the healthy subjects were
significantly younger than the patients with CHF (P<.001),
a comparison of Pes amplitude, which is the variable
showing the greatest difference between the two groups and is the
variable of greatest interest, in the four youngest and four oldest
healthy subjects (age, 31.8±0.9 versus 53.3±4.3 years) revealed
no
significant difference (5.7±0.8 versus 6.5±0.9 mm Hg,
P=.539). Similarly, within the group with CHF, the
Pes amplitude of the four youngest and four oldest patients
(53.5±1.3 versus 65.3±1.9 years) was not significantly different
(9.9±2.3 versus 8.5±1.1 mm Hg, P=.968). In
addition,
there was no significant correlation between age and Pes
amplitude in either the healthy group (r=.203,
P=.60) or the group with CHF (r=-.255,
P=.40) or within the combined healthy and CHF groups
(r=.265, P=.23). Accordingly, there was no
significant effect of age on Pes amplitude, and therefore
differences between the healthy subjects and the patients with CHF for
this variable are attributable to disease state. The peak inspiratory
LVPtm, systolic LVPtm, and
systolic LVPtmxheart rate at baseline were comparable
between groups.
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Effects of CPAP
Baseline values for all variables were
comparable on the time
control and CPAP days within the healthy and CHF groups. During the
time control, all variables remained constant over time in both groups.
In the post-CPAP recovery period, all variables returned to the time
control level except heart rate, which remained lower in the group with
CHF.
Healthy subjects experienced an increase in end-expiratory
Pes of 3.0 mm Hg (P<0.001) but no change in
the Pes amplitude (Figs 1
and 2).
Peak
inspiratory and systolic Pes both increased by 4.1 mm Hg
(P<.005) (Fig 3). Patients with CHF
experienced a 2.9 mm Hg increase in end-expiratory Pes
(P<.001), a 3.6 mm Hg reduction in mean Pes
amplitude (P<.025), a 6.1 mm Hg increase in peak
inspiratory Pes (P<.001), and a 5.3 mm Hg
increase in systolic Pes (P<.001) (Figs 1 through
3). Respiratory rate decreased in
the healthy group (-1.6
breaths per minute, P<.01) but not in the group with CHF
(Fig 4). Pes amplitudexrespiratory rate
decreased by 27% in those receiving CPAP in the healthy group (-22
mm Hgxbreaths per minute, P<.05) and by 40% in the group
with CHF (-76 mm Hgxbreaths per minute, P<.005).
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Systolic and diastolic blood pressures did not change significantly on
CPAP in either group (Fig 5). Because increases in peak
inspiratory and systolic Pes were offset by a slight
increase in systolic blood pressure in the healthy subjects, peak
inspiratory and systolic LVPtm (Fig 6) on
CPAP did not decrease. In contrast, the group with CHF experienced
reductions in both peak inspiratory and systolic LVPtm
(-6.1 mm Hg, P<.01, and -5.7 mm Hg,
P<.025,
respectively). Heart rate decreased with CPAP only in the group with
CHF (-5.2 beats per minute, P<.01, Fig 7).
Consequently, systolic LVPtmxheart rate decreased
significantly by 11% (-8.7 mm Hgxbeats per minute/100,
P<.005) in the CHF group but not in the healthy group.
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SVI
and CI decreased while on CPAP from 34.2±1.7 to 30.5±1.0
mL/m2 (P<.01) and from 2.20±0.14 to
1.96±0.14
L · min-1 · m-2
(P<.025),
respectively, among healthy subjects (Fig 8). In
contrast, SVI and CI did not change in the patients with CHF while on
CPAP. However, there was considerable variation in the response, with
approximately half experiencing an increase and half experiencing a
decrease in CI and SVI, as seen in previous
studies.1 2
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The primary purpose of the present study was to assess the effects of CPAP on intrathoracic pressure, as reflected by Pes, and on left ventricular afterload, as reflected by LVPtm, in healthy subjects and in patients with CHF. Three main observations were made. First, the amplitude of inspiratory Pes swings was greater in patients with CHF than in healthy subjects. These data indicate that inspiratory muscles of patients with CHF generate greater force than those of healthy subjects.17 19 20 Second, the more negative systolic Pes in the group with CHF contributed proportionally more to systolic LVPtm than it did in the healthy subjects. Third, among patients with CHF but not healthy subjects, increasing levels of CPAP were associated with progressive decreases in Pes amplitude, peak inspiratory and systolic LVPtm, and heart rate. CI did not change in patients with CHF. The clinical implications of our findings are that CPAP unloads the left ventricle and inspiratory muscles of patients with CHF without compromising CI.
Effects of CPAP on Pes
LVPtm is an
important determinant of left ventricular
afterload. In the present study, we used Pes to
estimate extracardiac pressure21 22 23
and to calculate peak
inspiratory and systolic LVPtm.6 24
Changes in
Pes have been shown to correlate closely with changes in
pleural and pericardial pressures during systole under a variety of
conditions.21 22 Therefore, changes in Pes
provide a reasonable estimate of change in
intrathoracic14 18 and systolic pericardial
pressures, if
not their absolute magnitudes. Pes amplitude provides a
good index of the degree of inspiratory muscle force generation and
energy expenditure per breath.17 18 The greater
Pes amplitude observed in patients with CHF agrees with
previous findings19 and probably contributes to
dyspnea.17 19 20 In the present study, we
used
Pes amplitudexrespiratory rate as an index of inspiratory
force generation over time.17 18 We found that
Pes amplitudexrespiratory rate was significantly greater
in the group with CHF than in the control group. These findings
indicate that the inspiratory muscles of patients with CHF generate
more force and would require a greater proportion of a lower CI to meet
their increased energy demands than would those of healthy
subjects.25
Two likely explanations for the high Pes amplitude in the group with CHF were that lung compliance was reduced or airway resistance increased due to interstitial and bronchial edema.8 19 26 In addition, the large Pes amplitude may have reflected a vagally mediated increase in ventilatory drive secondary to elevated pulmonary venous pressure.27 However, because we did not measure tidal volume or compliance, we cannot discuss the relative contribution of each of these factors to increased Pes amplitude.
The greater reduction in Pes amplitude in those receiving CPAP in the group with CHF than in the healthy group is interesting and suggests that the impact of CPAP may be amplified in the presence of increased lung water. This could occur, for example, if CPAP caused an extrathoracic redistribution of lung water leading to an increase in lung compliance7 28 29 30 or if it caused a reduction in tidal volume or an increase in lung volume to a more favorable position on the pressure-volume curve.28 31 Regardless of the mechanism, CPAP-induced reductions in Pes amplitude and Pes amplitudexrespiratory rate indicate that the inspiratory muscles were unloaded, thus reducing their energy demands.18 28 32
Effects of CPAP on LVPtm
Negative intrathoracic
pressure contributes to left ventricular
afterload by increasing
LVPtm.6 33 34
Therefore, the more negative systolic Pes in the group with
CHF had a relatively greater impact on systolic LVPtm than
in the healthy group. In contrast to the healthy heart, the failing
heart is very sensitive to changes in afterload, so hemodynamics are
more adversely affected by exaggerated negative intrathoracic
pressure.23 33 34 35 36
For example, exaggerated negative
intrathoracic pressure during obstructive sleep apneas probably
contributes to impaired myocardial function in patients with dilated
cardiomyopathy.3 Accordingly, the most important finding
of the present study was that under carefully controlled
conditions, CPAP caused consistent dose-related reductions in peak
inspiratory and systolic LVPtm in the group with CHF
secondary to increases in peak inspiratory and systolic
Pes. This contrasted with the lack of an effect on
LVPtm in healthy subjects, where small increases in
Pes while on CPAP were offset by slight increases in
systolic blood pressure (Figs 3, 5, and
6). What is remarkable is that
these effects of CPAP in the group with CHF were observed in addition
to afterload reduction by pharmacological
agents.37 38
Moreover, reductions in LVPtm secondary to CPAP resulted
from increases in Pes rather than decreases in systolic
blood pressure. This may well be one of the mechanisms responsible for
the long-term improvements in cardiac function we observed after
nightly application of CPAP to medically treated patients with CHF and
coexisting sleep apnea.3 4 5
The group with CHF experienced a significant fall in heart rate while receiving CPAP.2 10 This suggests that CPAP either reduced cardiac sympathetic or increased parasympathetic activity, directly or reflexively. However, a decrease in intrathoracic aortic transmural pressure due to CPAP would tend to decrease baroreceptor discharge. In addition, neither CI nor blood pressure changed in the group with CHF while receiving CPAP. Consequently, it is more likely that stimulation of pulmonary vagal afferents by CPAP-induced lung inflation increased parasympathetic tone and reflexively reduced cardiac sympathetic outflow.39 In contrast, in the healthy group, the sympathostimulatory effects of a reduced CI while receiving CPAP probably offset any sympathoinhibitory effects of lung inflation and accounted for the absence of any net change in heart rate.
CPAP caused reductions in SVI and CI in the healthy group but did not reduce afterload. Therefore, decreases in CI probably arose from CPAP-induced reductions in preload.7 9 22 40 41 In contrast, the group with CHF did not experience a decrease in SVI or CI while receiving CPAP. This finding is consistent with previous work showing that positive pressure breathing increases SVI and CI in patients with CHF and elevates left ventricular filling pressures but reduces SVI and CI in those whose filling pressures are normal.2 42 43 44 Approximately half of our patients with CHF experienced an increase in SVI and CI and the remainder experienced a decrease, resulting in no net change in SVI or CI. Because cardiac filling pressures were not measured, patients could not be separated into those with high and low preloads. However, a reasonable explanation for the absence of any increase in group mean values for SVI and CI in the patients with CHF is that the preload-reducing effect of CPAP offset the afterload-reducing effect in patients with low filling pressures.
Doppler estimates of stroke volume have been validated under experimental conditions similar to ours.41 45 Estimations of stroke volume by continuous wave Doppler yield measures of stroke volume that are as reliable and reproducible as those obtained by pulsed wave Doppler.46 In addition, we have shown that 10 cm H2O of CPAP does not affect aortic annular diameter, so time-velocity integrals measured in those receiving CPAP are unlikely to have been subject to artifactual influences. Although Doppler measurements tend to systematically underestimate the absolute stroke volume,47 they accurately reflect changes in stroke volume.41 45 46 47 48 49 Therefore, changes in SVI in response to CPAP in our subjects likely provide a reasonable estimate of the magnitude of change in this variable. Among the patients with CHF, CPAP caused a reduction in systolic LVPtmxheart rate (an index of myocardial systolic force generation and O2 consumption over time10 13 ). This effect, combined with the reduced Pes amplitudexrespiratory rate in those receiving CPAP, will reduce myocardial and inspiratory muscle energy demands, allowing redistribution of blood flow to other organs to better match their energy requirements. Moreover, the reduction in heart rate in the group with CHF could potentially improve subendocardial perfusion and allow for better left ventricular diastolic filling. Therefore, CPAP can improve cardiorespiratory efficiency in patients with CHF even in the absence of any increase in CI.
In summary, we have demonstrated that by increasing intrathoracic pressure, CPAP reduces left ventricle afterload and unloads the inspiratory muscles of patients with CHF. These findings may help to explain short- and long-term improvements in cardiorespiratory function that have been reported in patients with CHF while receiving CPAP.3 4 5 10 Further physiological studies will be required to determine other mechanisms whereby CPAP exerts these effects. Our findings also provide a strong rationale for examining the clinical usefulness of CPAP as a nonpharmacological method of reducing afterload in patients with CHF.
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Acknowledgments |
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This study was supported by operating grant MT 11607 from the Medical Research Council of Canada. Drs Naughton and Rahman are recipients of fellowships from the Medical Research Council of Canada. Drs Floras and Bradley are recipients of Career Scientist Awards from the Ontario Ministry of Health. The authors would like to acknowledge the technical assistance of Beverly Senn, RN, and Dean Benard, RN, in performing the experiments.
Received October 10, 1994; accepted October 18, 1994.
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