Transpulmonary pressure and lung volume of the cat and the newborn: removal of cardiac effects with a digital filter

1978 ◽  
Vol 16 (4) ◽  
pp. 397-407 ◽  
Author(s):  
S. Laxminarayan ◽  
A. J. G. Spoelstra ◽  
P. Sipkema ◽  
N. Westerhof
Keyword(s):  
Digital Filter ◽  
Lung Volume ◽  
Transpulmonary Pressure ◽  
Cardiac Effects

Airway closure and reopening assessed by the alveolar capsule oscillation technique

1996 ◽  
Vol 80 (6) ◽  
pp. 2077-2084 ◽  
Author(s):  
D. R. Otis ◽  
F. Petak ◽  
Z. Hantos ◽  
J. J. Fredberg ◽  
R. D. Kamm
Keyword(s):  
Lung Volume ◽  
Input Impedance ◽  
Transpulmonary Pressure ◽  
Closing Volume ◽  
Airway Closure ◽  
Breathing Cycle ◽  
Abrupt Increase ◽  
Consistent Effect ◽  
Peripheral Airways

An alveolar capsule oscillation technique was used to determine 1) the lobe pressure and volume at which airways close and reopen, 2) the effect of expiration rate on closing volume and pressure, 3) the phase in the breathing cycle at which airway closure occurs, and 4) the site of airway closure. Experiments were conducted in excised dog lobes; closure was detected by an abrupt increase in the input impedance of surfacemounted alveolar capsules. Mean transpulmonary pressure (Ptp) at closure was slightly less than zero (Ptp = -2.3 cmH2O); the corresponding mean reopening pressure was Ptp = 14 cmH2O. The expiration rate varied between 1 and 20% of total lobe capacity per second and had no consistent effect on the closing volume and pressure. When lung volume was cycled up to frequencies of 0.2 Hz, closure generally occurred on expiration rather than inspiration. These observations support the conclusion that mechanical collapse, rather than meniscus formation, is the most likely mechanism producing airway closure in normal excised dog lungs. Analysis of measured acoustic impedances and reopening pressures suggests that closure occurs in the most peripheral airways. Reopening during inspiration was often observed to consist of a series of stepwise decreases in capsule impedance, indicating a sequence of opening events.

Effect of parenchymal shear modulus and lung volume on bronchial pressure-diameter behavior

1978 ◽  
Vol 44 (6) ◽  
pp. 859-868 ◽  
Author(s):  
S. J. Lai-Fook ◽  
R. E. Hyatt ◽  
J. R. Rodarte
Keyword(s):  
Shear Modulus ◽  
Lung Volume ◽  
Pressure Difference ◽  
Transpulmonary Pressure ◽  
Pleural Pressure ◽  
Air Trapping ◽  
Control State ◽  
General Method

A method that interrelates lung pressure-volume behavior, bronchial pressure-diameter behavior, and parenchymal shear modulus is presented. The method was used to predict changes in intraparenchymal bronchial diameter that occurred when lobe pressure-volume behavior and parenchymal shear modulus were markedly changed by inducing air trapping in isolated dog lobes. Predictions agreed with measurements, thereby supporting the general method. Measured values for the shear modulus were approximately 0.7 times the transpulmonary pressure for the control state. Estimated values for the peribronchial pressure difference from pleural pressure during a deflation pressure-volume maneuver for transpulmonary pressures below 12 cmH2O were small, approximately +/- 1 cmH2O, its sign being positive or negative, depending on whether the bronchus was dilated or contricted.

High lung volume increases stress failure in pulmonary capillaries

1992 ◽  
Vol 73 (1) ◽  
pp. 123-133 ◽  
Author(s):  
Z. Fu ◽  
M. L. Costello ◽  
K. Tsukimoto ◽  
R. Prediletto ◽  
A. R. Elliott ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Lung Volume ◽  
Autologous Blood ◽  
Physiological Mechanism ◽  
Transpulmonary Pressure ◽  
Lung Volumes ◽  
Lung Inflation ◽  
Pulmonary Capillaries ◽  
Scanning Electron

We previously showed that when pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to test whether stress failure occurred more frequently at high than at low lung volumes for the same Ptm. Lungs of anesthetized rabbits were inflated to a transpulmonary pressure of 20 cmH2O, perfused with autologous blood at 32.5 or 2.5 cmH2O Ptm, and fixed by intravascular perfusion. Samples were examined by both transmission and scanning electron microscopy. The results were compared with those of a previous study in which the lung was inflated to a transpulmonary pressure of 5 cmH2O. There was a large increase in the frequency of stress failure of the capillary walls at the higher lung volume. For example, at 32.5 cmH2O Ptm, the number of endothelial breaks per millimeter cell lining was 7.1 +/- 2.2 at the high lung volume compared with 0.7 +/- 0.4 at the low lung volume. The corresponding values for epithelium were 8.5 +/- 1.6 and 0.9 +/- 0.6. Both differences were significant (P less than 0.05). At 52.5 cmH2O Ptm, the results for endothelium were 20.7 +/- 7.6 (high volume) and 7.1 +/- 2.1 (low volume), and the corresponding results for epithelium were 32.8 +/- 11.9 and 11.4 +/- 3.7. At 32.5 cmH2O Ptm, the thickness of the blood-gas barrier was greater at the higher lung volume, consistent with the development of more interstitial edema. Ballooning of the epithelium caused by accumulation of edema fluid between the epithelial cell and its basement membrane was seen at 32.5 and 52.5 cmH2O Ptm. At high lung volume, the breaks tended to be narrower and fewer were oriented perpendicular to the axis of the pulmonary capillaries than at low lung volumes. Transmission and scanning electron microscopy measurements agreed well. Our findings provide a physiological mechanism for other studies showing increased capillary permeability at high states of lung inflation.

Effect of volume and volume history of the lungs on pulmonary shunt flow

1964 ◽  
Vol 207 (1) ◽  
pp. 235-238 ◽  
Author(s):  
Nicholas R. Anthonisen
Keyword(s):  
Lung Volume ◽  
Total Lung Capacity ◽  
Full Range ◽  
Transpulmonary Pressure ◽  
Pulmonary Shunt ◽  
Shunt Flow ◽  
Lung Capacity ◽  
Surface Active Properties ◽  
History Of ◽  
Surface Active

Relative pulmonary shunt flow (Qs/Qt), was measured in denitrogenated open-chested cats during apnea over the full range of lung volumes. The particular lung volume and transpulmonary pressure were also measured. When completely collapsed lungs were inflated, Qs/Qt decreased sharply to 3% at total lung capacity (TLC). During deflation from TLC Qs/Qt was insensitive to changes in lung volume. Qs/Qt remained low during reinflation after deflation from TLC. These changes in shunt flow can be interpreted as due to either recruitment or collapse of gas exchange units during lung volume change. It appears that completely collapsed lungs inflate very unevenly but that deflation from TLC proceeds remarkably evenly. Reinflation after deflation from TLC also seems to proceed evenly, and the manifest pressure-volume hysteresis is most likely due to hysteresis of the surface-active properties of the alveolar lining material.

Trapped air in ventilated excised rat lungs

1976 ◽  
Vol 40 (6) ◽  
pp. 915-922 ◽  
Author(s):  
D. G. Frazer ◽  
K. C. Weber
Keyword(s):  
Stress Relaxation ◽  
Flow Rate ◽  
Lung Volume ◽  
Transpulmonary Pressure ◽  
Maximum Pressure ◽  
Lung Inflation ◽  
Minimum Pressure ◽  
Trapped Air ◽  
Rat Lungs ◽  
Reference Pressure

Degassed excised rat lungs were ventilated in a water-filled plethysmograph with the carina as the zero pressure reference. Pressure-volume curves were recorded from a minimum transpulmonary pressure (Pmin) of -5 cmH2O to a maximum pressure (Pmin) of 30 cmH2O. An index of the minimun volume for the lung (Vm) divided by the maximum lung volume for the same cycle (Vmax) was used as an index of the amount of air trapped within the lung. As the flow rate was decreased from 38.2 to 1.9 ml/min, there were significant increases in the amount of air trapped in the lung. As the maximum pressure was decreased to 25 and 20 cmH2O, or the minimum pressure was increased to 6 and 11 cmH2O, the amount of trapped air in the lung significantly decreased. The rate of lung inflation had a much greater influence on the amount of trapped air than either the deflation rate or stress relaxation. The results are consistent with the theory that bubbles are formed during inflation and are the main cause of air trapped in the excised lung.

Airway-parenchymal interdependence and bronchial responsiveness in two highly inbred rat strains

1993 ◽  
Vol 74 (2) ◽  
pp. 538-544 ◽  
Author(s):  
R. J. Dandurand ◽  
L. J. Xu ◽  
J. G. Martin ◽  
D. H. Eidelman
Keyword(s):  
Lung Volume ◽  
Bronchial Hyperresponsiveness ◽  
Transpulmonary Pressure ◽  
Volume Effect ◽  
Male Rats ◽  
Rat Strains ◽  
Response Curves ◽  
Bronchial Responsiveness ◽  
Inbred Rat Strains ◽  
Inbred Rat

To investigate if airway-parenchymal interdependence may account for differing bronchial responsiveness between inbred rat strains, Fisher and Lewis 12-wk-old male rats were anesthetized, tracheostomized, and placed in a pressure plethysmograph. Functional residual capacity, total lung capacity [lung volume at transpulmonary pressure (PL) of 30 cmH2O], and specific compliance were determined and were found to be similar. Rats were paralyzed and mechanically ventilated. Concentration-response curves were constructed by calculating lung resistance (RL) and lung elastance (EL) after nebulization of saline and then doubling doses of methacholine (0.0625–512 mg/ml). In Fisher (n = 8) and Lewis (n = 7) rats RL and EL were again determined at a lung volume corresponding to 2 cmH2O PL above FRC. The doubling, maximal, and half-maximal effective concentrations were determined for RL and EL. The doubling of effective concentrations of RL and EL were significantly less for Fisher rats. Other groups of Fisher (n = 5) and Lewis (n = 5) rats were similarly exposed to three concentrations of methacholine (64, 128, and 256 mg/ml), and determinations of RL and EL were made at lung volume corresponding to PL of 0, 2, 4, and 8 cmH2O. In both groups, Lewis rats exhibited a significant effect of volume on maximal RL and EL, whereas Fisher rats did not. The absence of volume effect on bronchoconstriction in the hyperresponsive Fisher strain is consistent with the hypothesis that altered airway-parenchymal interdependence contributes to bronchial hyperresponsiveness.

Pulmonary afferent control of breathing as end-expiratory lung volume decreases

1990 ◽  
Vol 68 (5) ◽  
pp. 2186-2194 ◽  
Author(s):  
J. F. Green ◽  
M. P. Kaufman
Keyword(s):  
Lung Volume ◽  
Breathing Pattern ◽  
Blood Gases ◽  
Transpulmonary Pressure ◽  
Stretch Receptor ◽  
Receptor Activity ◽  
Vagal Afferents ◽  
Vagal Nerves ◽  
Residual Capacity ◽  
Alpha Chloralose

We studied reflex changes in breathing elicited by graded reductions in end-expiratory lung volume (EEVL) and the vagal nerves responsible. The chests of nine dogs anesthetized with alpha-chloralose were opened, and the lungs were ventilated by a phrenic nerve-driven servo-respirator. The immediate effects of a 50% reduction in end-expiratory transpulmonary pressure (EEPtp) from control (EEVL equivalent to functional residual capacity) were to significantly increase both tidal volume (VT) and breathing frequency (f) from 0.402 +/- 0.101 to 0.453 +/- 0.091 liter (mean +/- SD) and 11.8 +/- 5.4 to 15.7 +/- 6.4 breaths/min, respectively (P less than 0.05). Further reductions in EEPtp to 0 cmH2O did not change VT but augmented f to 19.6 +/- 6.6 breaths/min (P less than 0.05). The increase in f as EEVL decreased was due entirely to a reduction in expiratory time. Vagotomy abolished these reflexes. By 90 s after reduction in EEVL, arterial PCO2 fell significantly and VT returned to or below control values. We therefore repeated these experiments in five dogs whose blood gases were controlled by cardiopulmonary bypass. There were no secondary changes in VT and by 90 s breathing pattern could be characterized as rapid and deep. In another eight dogs submitted to the same collapse protocol, we recorded action potentials from all known categories of pulmonary vagal afferents. These studies demonstrated that the changes in breathing pattern induced by a 50% reduction in EEPtp were due to a withdrawal of slowly adapting stretch receptor activity; however, continued increases in f as EEVL was reduced further were due to increases in rapidly adapting stretch receptor activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of chest compression on reflex ventilatory drive and pulmonary function

1962 ◽  
Vol 17 (4) ◽  
pp. 701-705 ◽  
Author(s):  
Malcolm B. McIlroy ◽  
John Butler ◽  
Theodore N. Finley
Keyword(s):  
Chest Compression ◽  
Lung Volume ◽  
Transpulmonary Pressure ◽  
Normal Subjects ◽  
Lung Compliance ◽  
External Compression ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Ventilatory Drive ◽  
Anatomical Dead Space

External compression of the chest sufficient to reduce the lung volume (FRC) by 1 liter in eight normal subjects interfered with the mechanical function of the lungs. We have confirmed the findings of Caro et al. ( J. Clin. Invest. 39: 573, 1960), who showed a decrease in lung compliance and an increase in respiratory rate. Neither returned to normal when the compressing force was removed, and it was not until the subject took a deep breath that the lungs returned to their control state. We also found a reduction in anatomical dead space and alveolar hyperventilation. Arterial blood gas tensions showed evidence of complex ventilation-perfusion abnormalities, which could not be explained by any single factor. We think the hyperventilation associated with chest compression is reflex in origin and related to a decrease in lung volume rather than to any change in transpulmonary pressure. Submitted on January 4, 1962

Relationship between regional lung volume and regional pulmonary vascular resistance

1982 ◽  
Vol 52 (4) ◽  
pp. 914-920 ◽  
Author(s):  
E. M. Baile ◽  
P. D. Pare ◽  
L. A. Brooks ◽  
J. C. Hogg
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Lung Volume ◽  
Regional Blood Flow ◽  
Transpulmonary Pressure ◽  
Simple Relationship ◽  
Volume Curve ◽  
Regional Lung ◽  
Residual Capacity

We have examined the relationship between regional pulmonary vascular resistance (PVRr) and regional lung volume (VLr) to determine whether the decrease in blood flow in the dependent lung (zone 4) was related to lung volume. Regional blood flow (Qr) was measured with radiolabeled macroaggregates at functional residual capacity (FRC) and at transpulmonary pressure of 10 cmH2O (PL10) in 10 anesthetized supine dogs. VLr was determined at FRC by measuring lung density in frozen lung slices and was calculated at PL10 using each dog's pressure-volume curve. We found that when PVRr was expressed as a function of VLr there was not a single relationship between the two. Instead we found two separate U-shaped curves, one at FRC and one at PL10 indicating that the increased vascular resistance at the lung base remained when the lung volume was made uniform by inflation to PL10. This suggests that there is no simple relationship between VLr and PVRr.

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