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1 Division of Anesthesiologic Investigations, University of Geneva, 1211 Geneva; 2 Division of Anesthesia, Geneva Children's Hospital, 1205 Geneva, Switzerland; 3 Department of Medical Informatics and Engineering, University of Szeged, Szeged 6720, Hungary; and 4 Division of Clinical Sciences, Institute for Child Health Research and Centre for Child Health Research, University of Western Australia, Perth 6008, Australia
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Changes in
pulmonary hemodynamics have been shown to alter the mechanical
properties of the lungs, but the exact mechanisms are not clear. We
therefore investigated the effects of alterations in pulmonary vascular
pressure and flow (
p) on the mechanical properties
of the airways and the parenchyma by varying these parameters
independently in three groups of isolated perfused normal rat lungs.
The pulmonary capillary pressure (Pcest), estimated from
the pulmonary arterial (Ppa) and left atrial pressure (Pla), was
increased at constant p (n = 7), or
p was changed at Pcest = 10 mmHg (n = 7) and at Pcest = 20 mmHg
(n = 6). In each condition, the airway resistance (Raw)
and parenchymal damping (G) and elastance (H) were identified from the
low-frequency pulmonary input impedance spectra. The results of
measurements made under isogravimetric conditions were analyzed. The
changes observed in the mechanical parameters were consistent with an
altered Pla: monotonous increases in Raw were observed with increasing
Pla, whereas G and H were minimal at Pla of ~7-10 mmHg and
increased at lower and higher Pla. The results indicate that Pla, and
not Ppa or p, is the primary determinant of the
mechanical condition of the lungs after acute changes in pulmonary
hemodynamics: the parenchymal mechanics are impaired if Pla is lower or
higher than physiological, whereas airway narrowing occurs at high Pla.
respiratory mechanics; forced oscillations; pulmonary circulation
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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PREVIOUS STUDIES
HAVE DEMONSTRATED that changes in pulmonary hemodynamic
conditions alter the mechanical properties of the lungs
(1-3, 5-7, 9-11, 13, 15, 19-24,
26-28). A compromised lung function has been observed in
clinical situations involving an abnormally high pulmonary blood flow
(p) (9, 11, 13, 22, 24) and/or an
elevated pulmonary arterial pressure (Ppa) (1-3, 5, 6, 20,
23, 26-28). Nevertheless, the results of these previous
studies lead to inconsistent conclusions as to which of the pulmonary
hemodynamic parameters has the dominant effect on lung mechanics.
The elevated p has been reported to be the primary
cause of the decreased lung compliance (CL) in adults with
cardiac failure (11) and in children with congenital heart
disease (13, 22, 24), although normal CL
values have also been found in children with a high
p and a normal Ppa (2, 15). Conversely,
a high Ppa has been demonstrated to play a major role in determining the mechanical properties of the lungs, since changes were observed only when Ppa was elevated (2, 15, 27, 28). Finally, other
authors observed abnormal lung function only when an increased p was associated with an elevated Ppa (3,
20).
Many factors may contribute to these discrepancies, including the
complex nature of heart diseases, different underlying clinical conditions, or timing and methodological differences between the studies. Additionally, the clinical settings do not allow separate alterations of Ppa or p, and accordingly the primary
cause of the compromised lung function cannot be identified. Finally,
these previous studies used global parameters to characterize the
mechanical status of the lungs, and their results therefore combined
the contributions from the airways and the respiratory tissues.
In clinical practice, it is possible to influence the pulmonary
hemodynamic parameters relatively selectively by pharmacological means;
hence, it is important to clarify the mechanism responsible for the
adverse changes in lung mechanics. We therefore set out to investigate
the effects of acutely altered left atrial pressure (Pla), Ppa, and
p on the mechanical properties of the airways and
the parenchyma before the onset of edema by varying these parameters independently.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Animal preparation and isolated lung harvesting. Experiments were performed on 20 adult male Sprague-Dawley rats weighing 360-390 g. The rats were anesthetized with isoflurane via a facemask (3% induction, 1.4% maintenance dose), tracheotomized with a polyethylene cannula (14-gauge, Braun, Melsungen, Germany), and mechanically ventilated (model 683, Harvard Apparatus, South Natick, MA) with a tidal volume of 7 ml/kg and a respiratory rate of 70-80/min while a positive end-expiratory pressure of 2.5 cmH2O was maintained. Respiratory gases were monitored in the expiratory circuit of the ventilator (Ultima, Datex/Instrumentarium, Helsinki, Finland). Airway opening pressure was measured continuously (DP 45 transducer and 2D15 carrier demodulator, Validyne, Northridge, CA).
The femoral vessels were cannulated with a 28-gauge catheter (Portex, Hythe, UK) for blood sampling and continuous arterial blood pressure monitoring with a pressure transducer (model 156 PCE 06-GW2, Honeywell, Zurich, Switzerland). The rats were fully anticoagulated with heparin (1.5 IU/g). Thirty-five ml of blood diluted in colloid solution were then gently withdrawn over 5 min via the arterial cannula, while the collected blood was continuously replaced by an intravenous infusion of colloid solution (6% hydroxyethyl starch solution). A constant intravascular volume and a mean systemic blood pressure >50 mmHg were maintained by this maneuver to minimize the risk of lung ischemic lesions. The collected diluted blood was centrifuged (4,000 rpm for 10 min), and 17 ml of plasma were extracted. The resulting concentrated blood with a hematocrit of ~35% served as priming perfusate. A midline sternotomy was performed, and the chest was widely retracted. A polyethylene catheter (14 gauge, Braun) was placed into the main pulmonary artery via the right ventricular outflow track, advanced to immediately below its bifurcation, and connected to medical-grade silicone rubber tubing (1.47 mm ID, Ulrich, St. Gallen, Switzerland). The left ventricle and the left atrium were then widely opened, allowing free outflow of the remaining blood and resulting in complete exsanguination and the death of the animal. The lungs were immediately flushed through the pulmonary artery cannula with 30 ml of cold (10°C) hydroxyethyl starch 6% solution from a height of 30 cm to minimize the warm ischemic time period until reperfusion. Another catheter was placed in the left ventricle through the left ventriculotomy, in which a Combifix Adapter (Braun) was tightly fixed and connected to medical-grade silicone rubber tubing. Finally, a third catheter (polyethylene tubing, ID 0.88 mm, Portex) was introduced directly into the left atrium for the measurement of Pla. The surgical preparations were performed in a sterile manner. The lungs and the heart were extracted in a single block, dissected free of adjacent tissue, and weighed.Perfusion of the isolated lungs.
The experimental setup is shown schematically in Fig.
1. In a thermostabilized, humidified
Plexiglas chamber, the heart-lung block was suspended from an isometric
force displacement transducer (model FT03, Grass Instruments, Quincy,
MA), which continuously measured weight changes. The lungs were
ventilated with room air mixed with 5% CO2, and a
respiratory rate of 50/min, a tidal volume of 7 ml/kg, and a positive
end-expiratory pressure of 2.5 cmH2O were maintained.
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p. The priming volume of the tubing and reservoirs was 18 ml.
The mean Ppa and Pla were recorded continuously with pressure
transducers (model 156-PC 06-GW2, Honeywell) zeroed at the level of the
lung hilus. Pulmonary vascular resistance (Rv) was calculated as
follows: Rv = (Ppa 
Pla)/p. Pulmonary
microvascular pressure (Pcest) was estimated by applying
the Gaar equation (14): Pcest = Pla + 0.44 × (Ppa Pla). Weight, Ppa, Pla, and
p were sampled at a rate of 50 Hz by an
analog-to-digital converter. These signals, together with the
calculated Pcest, were displayed continuously by data
acquisition software (Biopac, Santa Barbara, CA) and stored on a
microcomputer (AST, Limerick, Ireland).
The temperature and pH of the perfusate were measured with a pH meter
(model 691, Metrohm, Herisau, Switzerland). The pH was maintained
between 7.35 and 7.45 and corrected with sodium bicarbonate or a change
of the inspired CO2 if this was indicated by the blood-gas analysis (model 505, Acid Base Laboratory, Copenhagen, Denmark). Steady-state gas exchange was confirmed by the stable
PO2, PCO2, and
hematocrit levels during the experiments.
Measurement of airway and parenchymal mechanics. The respective contributions of the airways and tissues to the total lung resistance were estimated by measuring the forced oscillatory impedance of the isolated lungs (ZL), as described previously (25). Briefly, the tracheal cannula was connected from the respirator to a loudspeaker-in-box system at end expiration. The loudspeaker generated a small-amplitude pseudorandom signal with frequency components between 0.5 and 21 Hz through a polyethylene wave tube with known geometry. Two identical pressure transducers (model 33NA002D, ICSensors, Milpitas, CA) were used for measurement of the lateral pressures at the loudspeaker and at the tracheal end of the wave tube. ZL was calculated as the load impedance of the wave tube (29).
To separate the airway and tissue mechanics, a model containing a frequency-independent airway resistance (Raw) and inertance (Iaw) in series with a constant-phase tissue compartment (18), including parenchymal damping (G) and elastance (H), was fitted to the ZL spectra by minimizing the relative differences between the measured and modeled impedance values (18). Tissue hysteresivity was calculated as follows:
= G/H
(12).
The load impedance of the endotracheal tube and the connecting tubing
was also determined, and the Raw and Iaw values were corrected by
subtracting the instrumental resistance and inertance values from them.
Study protocol.
After the start of the perfusion, a period of 20-30 min was
allowed for the respiratory and hemodynamic variables to establish steady-state conditions and for the preparation to become
isogravimetric. If isogravimetric conditions were not reached within 30 min of perfusion or if p was <5 ml/min at normal
Ppa and Pla values, the lungs were excluded (this occurred in <10% of
the experiments because of technical problems in the surgical preparation).
p was
constant. Four to six ZL recordings were made and ensemble
averaged every 20 min.
In another group of lungs (n = 7), the perfusion of the
lungs was established by applying normal levels of Ppa (17.5 mmHg) and
Pla (7.5 mmHg). The resulting flow (5-6 ml/min) was then kept constant for each lung during the experiments, while the mean Pcest was altered from 5 to 25 mmHg in steps of 5 mmHg.
This was accomplished by elevating the perfusion reservoir to increase Ppa and simultaneously adjusting Pla through elevation of the outflow
level of the left ventricular cannula to a sufficient height.
In the next group of lungs (n = 7),
p was doubled stepwise from 2.5 to 15 ml/min, while
the mean Pcest was kept at an approximately physiological
value of 10 mmHg to investigate the role of the altered
p on the lung mechanics. In this group, elevation of the perfusion reservoir was associated with a lowering of the outflow
level of the left ventricular cannula.
Finally, p was altered while Pcest was
kept abnormally high. In these lungs (n = 6), a
Pcest of 20 mmHg was set after the perfusion had reached
the steady state, and p was decreased from 30 ml/min
in 5 ml/min steps until a p of 5 ml/min was
achieved, and it was then decreased to 2.5 ml/min. This was
accomplished by decreasing and increasing the heights of the perfusion
reservoir and the outflow of the left ventricular catheter,
respectively. The changes in p made it necessary to
alter the blood volume delivered by the roller pump into the perfusion reservoir.
A period of 5-10 min was necessary in all lungs to establish the
steady-state conditions after a change in Pcest or
p. Four to six ZL recordings were
collected thereafter in each hemodynamic condition and were ensemble
averaged. The weight gain was calculated during ZL
measurements, i.e., when steady-state conditions had been established,
and it was used as an edema index. There was no statistically
significant difference in the size of the lungs in the various protocol groups.
Statistical analysis. Scatters in the parameters were expressed in SE values. We used one-way analysis of variances with the Student-Newman-Keuls multiple comparison procedure to compare the lung mechanical parameters under different hemodynamic conditions. Each test was performed with a significance level of P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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None of the mechanical parameters in the control lungs exhibited a
statistically significant change. After 2 h of perfusion, the
relative changes in Raw, Iaw, G, and H were 1.0 ± 5.2%,
5.9 ± 2.2%, 3.9 ± 2.6%, and 3.3 ± 2.2%,
respectively. No signs of edema development were detected in these
lungs, since the weight gain values were not statistically
significantly different from zero (0.05 ± 0.12 mg/min,
P = 0.51 after 2 h of perfusion).
Figure 2 summarizes the results obtained
at different levels of Pcest while p was
kept constant. The accumulation of extravascular fluid did not
contribute to the changes observed in the mechanical parameters until
Pcest = 20 mmHg was reached; increases in weight gain
were evident only at Pcest = 25 mmHg. Increasing
Pcest caused gradual increases in Raw, which reached
statistically significant levels at >15 mmHg. The highest relative
change in Raw before edema development was 22.1 ± 7.8% (at 20 mmHg) compared with the value at the physiologically normal
Pcest of 10 mmHg. No systematic change was observed in Iaw
in response to changes in Pcest. G and H responded to the
altered Pcest with similar patterns of change: they were
minimal at Pcest = 10 mmHg and exhibited statistically significant increases at lower (20.9 ± 4.5% for G and 17.1 ± 4.2% for H at 5 mmHg) and higher Pcest values
(26.9 ± 3.4 and 26.7 ± 5.5%, respectively, at 20 mmHg).
The similar changes in G and H resulted in fairly constant values.
Rv was highest at Pcest = 5 mmHg; it decreased
slightly at higher Pcest.
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The changes recorded in the parameters when p was
altered at Pcest = 10 mmHg are illustrated in Fig.
3. Edema did not develop in this group at
any level of p. No statistically significant changes
occurred in the airway parameters; the maximal relative changes in Raw
and Iaw were 32.3 ± 15.1 and 30.5 ± 11.5%, respectively. Increasing p caused gradual increases in the
parenchymal parameters; the changes became statistically significant at
10 ml/min for G and 12.5 ml/min for H. The maximal relative changes
were 35.8 ± 4.1 and 19.4 ± 4.1% for G and H, respectively.
The relatively greater increases in G resulted in small, but
statistically significant, increases in from
p = 7.5 ml/min. Although there was a tendency for Rv to increase with p, this effect was not
statistically significant.
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Figure 4 illustrates the parameters at
different levels of p when Pcest was
kept at 20 mmHg. No edema developed at high p
levels, whereas marked increases in weight gain were observed at
p = 5 and 2.5 ml/min (note that the experiments
were started at p = 30 ml/min). Monotonous and
statistically significant elevations in Raw were obtained with
decreasing p, with a maximal relative change
of 48.3 ± 13.5% before edema development. No systematic changes
were observed in Iaw with changing p. G and H
exhibited monotonous increases with decreasing p;
significant changes were observed in both parameters from 15 ml/min,
and the maximal elevations before edema development were 29.2 ± 7.8 and 28.2 ± 6.4% for G and H, respectively. Alteration of
p did not have a significant effect on or Rv.
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Figure 5 depicts the relationships
between Ppa and weight gain and between Ppa and the mechanical
parameters for all the lungs in the groups, where the vascular
pressures (Ppa and/or Pla) or p were altered.
Pooling of the data points obtained in the three groups did not reveal
any clear relationship between Ppa and weight gain. Likewise, no
correlation was obvious between Ppa and the lung mechanical parameters.
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The relationships between Pla and weight gain and between Pla and the
lung mechanical parameters for all the lungs in which the pulmonary
hemodynamics were altered are outlined in Fig.
6. Weight gain remained at around zero at
Pla < 10 mmHg, and it was generally positive at Pla > 20 mmHg. No clear effects of Pla on Raw were evident at low Pla levels;
however, systematically higher Raw values were observed at higher Pla.
G and H were minimal at Pla ~ 7-10 mmHg, whereas these
parameters were markedly higher at lower and higher Pla.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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In the present study, the flow and pressures in the pulmonary circulation were varied independently, and the resulting changes in the airway and parenchymal mechanics were systematically investigated. We observed significant changes in the mechanical properties of the airways and the parenchyma in response to acute alterations of the pulmonary hemodynamic parameters, with characteristically different patterns of change in the various groups.
Methodological issues. The isolated, perfused rat lung model offers ideal conditions under which to investigate how acute changes in pulmonary hemodynamics alter the mechanical conditions of the lungs. In this experimental setting, each pulmonary hemodynamic parameter can be altered independently, and the acute changes in lung mechanics can be assessed in the absence of confounding systemic hormonal and neurogenic influences (31).
It has previously been demonstrated that it is primarily the pressure in the pulmonary capillaries that determines the pulmonary capillary filtration coefficient (14). Accordingly, the effective pulmonary capillary pressure (Pceff) influences the capillary permeability (16) and is expected to affect the viscoelastic properties of the alveolar wall via a direct mechanical interdependence. Direct techniques to measure Pceff, such as micropuncture (4) or analyses of the pulmonary occlusion pressure profile (17), are very difficult in the lungs of small rodents. We therefore applied an indirect technique in the present study and estimated Pceff by calculating Pcest from Ppa and Pla (14). Because this approach assumes that the venous resistance is ~44% of the total Rv (14), it is possible that changes in Rv might have biased the estimation of Pceff (8). We note, however, that Rv was fairly stable throughout the experiments, except when an extremely low Pla was associated with a subnormal Ppa (Fig. 2). The aim of the study was to investigate the effects of acute changes in the pulmonary hemodynamics on the mechanical properties of the lungs. Changes induced in the pulmonary vasculature by chronic heart-lung diseases, such as thickening of the pulmonary vasculature (30), did not fall in the scope of this study. Although acute and chronic effects are involved in clinical situations, the immediate improvement in lung function after surgery for congenital heart diseases (1, 3, 15, 20, 22, 24) suggests that acute effects play a significant role in the compromised lung function.Relationship between Ppa and lung mechanics. We did not find any coherent relationships between the lung mechanical parameters and Ppa (Fig. 5); the normal airway and parenchymal properties were maintained even at very high levels of Ppa (40-45 mmHg). Consequently, our data suggest that Ppa is not the primary variable determining the mechanics of the airways or the parenchyma after acute changes in pulmonary hemodynamics.
Previous studies led to inconsistent conclusions as concerns the relationship between Ppa and lung mechanics. Some investigations have revealed a clear correlation between an elevated Ppa and the subsequent changes in the mechanical properties of the lungs (2, 13, 23, 27, 28), although the increases in Ppa were always associated with increases in pulmonary venous pressures in those investigations. Other studies failed to detect any change in lung function in the presence of an elevated Ppa (3, 6, 7, 11, 22, 26). The findings of the present study are in accord with the latter observations, demonstrating only poor quantitative relationships between Ppa and the lung mechanical parameters.Relationship between Pla and lung mechanics. Plots of the parameter values against Pla reveal consistent relationships between the postcapillary pressure and the mechanical conditions of the airways and the parenchyma (Fig. 6). At low pulmonary venous pressures, no adverse effect on the airway mechanics was observed, whereas the parenchymal parameter values increased. At high Pla levels, the decreases in the overall airway diameter are associated with impairments of the parenchymal viscoelastic properties.
To our knowledge, the present study is the first to demonstrate an elevated parenchymal impedance at Pla levels lower than physiological. The mechanism by which a decreased Pla affects lung mechanics can only be hypothesized. The absence of a venous afterload pressure in the pulmonary circulation may result in a decreased tension in the pulmonary microcirculation, which may lead to an unstable geometry of the alveolar space. Without the tethering effect of the tense microvasculature, the alveolar units will tend to lose their geometric stability, which may lead to increased G and H. However, our finding that Raw was not elevated at low Pla levels suggests that these changes occurred only in the alveolar units and were not reflected in the measurements of Raw, a parameter determined by the geometry of the bronchial tree. The increases in G and H with Pla above physiological levels may be attributed to different phenomena. Deteriorated parenchymal mechanics my result from the increased tension of the pulmonary microvasculature, which may lead to an increased stiffness and dissipation of the parenchyma via mechanical attachment (2). Additionally, the decreases in functional lung volume at high vascular pressures might also have contributed to these changes (11): the blood-filled pulmonary microvasculature might have partially occupied the functional alveolar air space. Finally, the edema development further amplified the deterioration in airway and parenchymal mechanics when increases in weight gain were observed. Conflicting results have been reported on the effects of an altered Pla on lung mechanics. In agreement with our findings, the primary importance of the pulmonary venous pressure in the compromised lung function has been recognized by virtue of experimental studies performed on dogs (6, 19, 21). Nevertheless, these studies were limited to extremely high Pla levels (30-35 mmHg), and hence edema development was likely to be the major contributor to the observed changes in CL and RL (6) or in Raw (19, 21). In contrast, no clear relationships were observed between Pla and CL (2, 13) or between Pla and Raw (13) in children with congenital heart disease. This controversy can most probably be attributed to the relatively small range of Pla encountered in clinical studies (9-16 mmHg in Ref. 13), which leads to the rather moderate changes being undetected.p and lung mechanics.
Our experiments involving changing p revealed that
the mechanical properties of the lungs depend on the pressure
conditions maintained in the pulmonary vasculature during these
maneuvers. In the lungs where Pcest was maintained at 20 mmHg, the increases in Raw paralleled the increases in Pla. Moreover,
changes in p induced quantitatively similar, but
opposite, changes in the parenchymal mechanics at Pcest of
10 and 20 mmHg (Figs. 3 and 4). Although the sequences of
p levels were also opposite in these groups, a role
of the experimental time in these changes can be excluded, since the
mechanical parameters in the control group were stable. It seems far
more likely that the changes in Pla are responsible for this finding,
and the relationships between Pla and the lung mechanical parameters
explain this phenomenon as follows.
p at
Pcest = 10 mmHg corresponds to conditions of no change
in weight gain or Raw, while decreases in Pla cause increases in G and
H. In contrast, the impedance parameters of the lungs in which
p was altered at Pcest = 20 mmHg
are situated at the top of the U-shaped curve, where increasing Pla
causes increases in Raw, G, and H. Consequently, our results indicate
that Pla, and not p, triggers the changes in the
mechanical properties of the lungs. In this regard, it is noteworthy
that at extremely high flows (5 times higher than normal) lung
mechanics remain entirely normal, even if these p
values are associated with considerable elevations in Ppa, provided
that the Pla values are physiological.
Previous studies have emphasized the importance of an increased
p in the altered pulmonary mechanics (9, 13,
22). In other reports, it was found that an elevated
p affects lung mechanics only when high pulmonary
vascular pressures are also present (2, 3, 20, 26). The
conclusions of all these previous investigations were based on
measurements in children with various congenital heart diseases
(2, 3, 13, 20, 22, 26) or after administration of a
pulmonary vasodilator drug (9). Nevertheless, because the
changes in p were always associated with changes in
pulmonary pressures in those studies, it is difficult to identify the
separate roles of the abnormal pulmonary circulatory pressure and
flow from the measurements. Indeed, in agreement with our findings,
changes in p alone without modification of the
pressure conditions in the pulmonary circulation proved to have only
minor effects on the lung mechanics under experimental conditions
(6).
Summary and conclusions. In an isolated-perfused rat lung model, we demonstrated that acute changes in pulmonary hemodynamics lead to characteristic alterations in the mechanical properties of the airways and the parenchyma. The pulmonary hemodynamics variable to which changes in edema index and lung mechanical parameters can be related most consistently is Pla. Airway narrowing occurs only if Pla exceeds physiological values, whereas the parenchymal impedance parameters are minimal in the normal physiological range of Pla (7-10 mmHg) and exhibit parallel increases at lower and higher pressures. Because it is possible in clinical situations to alter the pulmonary hemodynamic parameters relatively independently by means of selective pharmacological interventions, the results of the present study indicate that maintenance of the physiological range of pulmonary venous pressure is a prerequisite for the optimal mechanical conditions of the lungs.
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ACKNOWLEDGEMENTS |
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This study was supported by Swiss National Science Foundation Grant 3200-056717.99/1 and Hungarian Scientific Research Fund Grant OTKA T30670.
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FOOTNOTES |
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Address for reprint requests and other correspondence: F. Peták, Div. of Anesthesiologic Investigations, University of Geneva, 1, rue Michel-Servet, CH-1211 Geneva, Switzerland (E-mail: Ferenc.Petak{at}medecine.unige.ch).
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 11 July 2001; accepted in final form 27 August 2001.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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