Vascular and airway pressures, and intersititial edema, affect peribronchial fluid pressure

1980 ◽  
Vol 48 (1) ◽  
pp. 177-185 ◽  
Author(s):  
H. Inoue ◽  
C. Inoue ◽  
J. Hildebrandt
Keyword(s):  
Lung Volume ◽  
Negative Pressure ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Pleural Pressure ◽  
Lung Edema ◽  
Lung Weight ◽  
Vascular Volume ◽  
Lobar Bronchus ◽  
Additional Lobes

Peribronchial-perivascular fluid pressure (Px(f) was measured relative to pleural pressure in six freshly excised dog lobes. Rapidly equilibrating saline-filled open-end catheters were inserted between lobar bronchus and artery to depths of 3 cm from the hilum. Px(f) was -4 to -8 cmH2O at resting lung volume and became more negative as transpulmonary pressure (Ptp) was increased, and less negative as vascular volume was increased. For example, at constnat Ptp = 30 cmH2O, mean Px(f) rose, respectively, from -35 to -31, -24, -16, and -4 cmH2O, as vascular pressure (Ppa/pv) was increased from -15 to 0, +10, +20, and +30 cmH2O. Lung weight rose steadily at Ppa/pv above 10, reflecting the development of edema. Px(f) had a significant hysteresis with respect to Ptp, being more negative in deflation. As lung edema developed, Px(f) became progressively less negative or slightly positive (even at high Ptp and low Ppa/pv) and hysteresis diminished. Modified wick catheters employed in four additional lobes gave similar results.These data suggest that Px(f) is strongly influenced by bronchovascular-parenchymal interdependence, and that when regions with negative Px(f) absorb fluid the negative pressure may be eliminated.

Effect of negative-pressure inflation of the lung on pulmonary vascular resistance

1961 ◽  
Vol 16 (3) ◽  
pp. 451-456 ◽  
Author(s):  
Lewis J. Thomas ◽  
Zora J. Griffo ◽  
Albert Roos
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Lung Volume ◽  
Negative Pressure ◽  
Transpulmonary Pressure ◽  
Absolute Magnitude ◽  
Pleural Pressure ◽  
Dog Blood ◽  
The Absolute ◽  
Static Conditions

Pulmonary vascular resistance was studied as a function of both transpulmonary pressure and lung volume, using excised dog lungs inflated by lowering pleural pressure and perfused with fresh, heparinized dog blood. The absolute magnitude of the vascular pressures was kept constant. Measurements were taken under static conditions. In all cases, resistance was found to be lowest at approximately half maximal lung volume and showed a progressive rise on either further inflation or further deflation. Also, the course of resistance as a function of transpulmonary pressure was found to vary significantly according to inflation history, especially inflation vs. deflation, but was found to be relatively constant when plotted against lung volume. It is thus concluded that pulmonary vascular resistance is volume-dependent rather than pressure-dependent when inflation is accomplished by lowering the pressure around the lung. Submitted on September 19, 1960

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.

Pressure-volume behavior of perivascular interstitium measured in isolated dog lung

1980 ◽  
Vol 48 (6) ◽  
pp. 939-946 ◽  
Author(s):  
S. J. Lai-Fook ◽  
B. Toporoff
Keyword(s):  
Interstitial Fluid ◽  
Venous Pressure ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Interstitial Fluid Pressure ◽  
Alveolar Pressure ◽  
Lung Weight ◽  
Lung Volumes ◽  
Water Accumulation ◽  
Alveolar Surface

Pulmonary perivascular interstitial fluid pressure (Px) was measured as a function of extravascular water accumulation (W). Px was measured directly by wick catheters and open-ended needles inserted in the interstitium near the hilus of isolated perfused dog lobes. Lobes were studied at constant transpulmonary pressure (Ptp) and vascular pressure (Pv, arterial equal to venous pressure). Px-W behavior had two distinct phases: an initial low compliance phase interpreted as perivascular filling, followed sometimes by an abrupt transition to a high compliance phase interpreted as alveolar flooding. W at transition was between 20 and 50% of the initial lung weight. Perivascular compliance during filling at a Ptp of 6 cmH2O was 0.1 g.g wet lobe wt-1.cmH2O-1, which was one-sixth that during alveolar flooding and 2.5 times that at a Ptp of 25 cmH2O. At the start of alveolar flooding, estimated alveolar interstitial fluid pressure was slightly (2 cmH2O) below alveolar pressure (PAlv) at a Ptp of 6 cmH2O but considerably belov PAlv at high lung volumes. These findings support the concept that alveolar surface tension reduces the interstitial fluid pressure below PAlv.

Mechanical Power and Development of Ventilator-induced Lung Injury

2016 ◽  
Vol 124 (5) ◽  
pp. 1100-1108 ◽  
Author(s):  
Massimo Cressoni ◽  
Miriam Gotti ◽  
Chiara Chiurazzi ◽  
Dario Massari ◽  
Ilaria Algieri ◽  
...  
Keyword(s):  
Lung Injury ◽  
Respiratory Rate ◽  
Transpulmonary Pressure ◽  
Lung Parenchyma ◽  
Plateau Pressure ◽  
Mechanical Power ◽  
Lung Edema ◽  
Lung Weight ◽  
Ventilator Induced Lung Injury ◽  
Power Threshold

Abstract Background The ventilator works mechanically on the lung parenchyma. The authors set out to obtain the proof of concept that ventilator-induced lung injury (VILI) depends on the mechanical power applied to the lung. Methods Mechanical power was defined as the function of transpulmonary pressure, tidal volume (TV), and respiratory rate. Three piglets were ventilated with a mechanical power known to be lethal (TV, 38 ml/kg; plateau pressure, 27 cm H2O; and respiratory rate, 15 breaths/min). Other groups (three piglets each) were ventilated with the same TV per kilogram and transpulmonary pressure but at the respiratory rates of 12, 9, 6, and 3 breaths/min. The authors identified a mechanical power threshold for VILI and did nine additional experiments at the respiratory rate of 35 breaths/min and mechanical power below (TV 11 ml/kg) and above (TV 22 ml/kg) the threshold. Results In the 15 experiments to detect the threshold for VILI, up to a mechanical power of approximately 12 J/min (respiratory rate, 9 breaths/min), the computed tomography scans showed mostly isolated densities, whereas at the mechanical power above approximately 12 J/min, all piglets developed whole-lung edema. In the nine confirmatory experiments, the five piglets ventilated above the power threshold developed VILI, but the four piglets ventilated below did not. By grouping all 24 piglets, the authors found a significant relationship between the mechanical power applied to the lung and the increase in lung weight (r2 = 0.41, P = 0.001) and lung elastance (r2 = 0.33, P < 0.01) and decrease in Pao2/Fio2 (r2 = 0.40, P < 0.001) at the end of the study. Conclusion In piglets, VILI develops if a mechanical power threshold is exceeded.

Perivascular interstitial fluid pressure measured by micropipettes in isolated dog lung

1982 ◽  
Vol 52 (1) ◽  
pp. 9-15 ◽  
Author(s):  
S. J. Lai-Fook
Keyword(s):  
Interstitial Fluid ◽  
Fluid Pressure ◽  
Transpulmonary Pressure ◽  
Alveolar Pressure ◽  
Lung Weight ◽  
Lung Inflation ◽  
Water Accumulation ◽  
The Right ◽  
Alveolar Surface ◽  
Lung Lobes

Micropipettes in conjunction with a servo-nulling system were used to measure fluid pressure (Pf) in the interstitium around the partially exposed vein near the hilus of the right upper lung lobes of the dog. Lobes were studied at constant transpulmonary pressure (Ptp). In the absence of extravascular water accumulation, Pf was -1.5 cmH2O relative to pleural pressure at Ptp of 6 cmH2O and vascular pressure (Pv) of 0 cmH2O and was more negative in lobes tested at higher Ptp values. In five lobes made edematous with plasma at Ptp of 6 cmH2O and Pv of 15 cmH2O, mean Pf increased from -1 to 4.4 cmH2O as lung weight increased up to 400% of the initial excised weight. In four other lobes, at Ptp of 15 cmH2O and Pv of 20 cmH2O, Pf increased from -2.4 to 8.8 for a similar increase in weight. In lobes degassed and filled with saline or plasma, Pf always equilibrated to alveolar pressure (PA). Results suggest that alveolar surface tension (tau) in air-filled lobes with gross edema prevented Pf from reaching PA. Reduction in Pf below PA was larger at higher Ptp, consistent with increased tau with lung inflation.

Respiratory mechanics in normal hamsters

1976 ◽  
Vol 40 (6) ◽  
pp. 936-942 ◽  
Author(s):  
K. W. Koo ◽  
D. E. Leith ◽  
C. B. Sherter ◽  
G. L. Snider
Keyword(s):  
Body Weight ◽  
Chest Wall ◽  
Transpulmonary Pressure ◽  
Pleural Pressure ◽  
Pressure Curve ◽  
Airway Closure ◽  
Lung Weight ◽  
Lung Volumes ◽  
Residual Capacity ◽  
Male Golden Hamsters

Lung volumes and quasi-static deflation volume-pressure relationships were measured in male golden hamsters anesthetized with pentobarbital. Volume was measured with a pressure plethysmograph, and pleural pressure was estimated by the use of a water-filled esophageal catheter. Mean body weight +/- SE was 122.3 +/-3.0 g, mean lung weight was 0.74 +/- 0.2 g or about 0.6% of body weight. Mean lung volume at 25 cmH2O transpulmonary pressure (TLC25) was 7.2 +/- 0.14 ml, 9.78 +/- 0.17 ml/g lung weight or 5.92 +/- 0.06 ml/100 g body weight. Mean functional residual capacity was 2.4 +/- 0.06 ml or 33.3% of TLC25. Mean vital capacity was 5.2 +/- 0.13 ml. Mean quasi-static compliance of lung was 0.63 +/- 0.03 ml/cmH2O. Chord compliance of chest wall between lung volumes of 1 and 4 ml above RV was 3.39 +/- 0.53 ml/cmH2O. At FRC, the chest wall recoiled inward, so that pleural pressure was positive (1.4 +/- 0.13 cmH2O) and the lung was resisting further collapse. The slope of the lung′s deflation volume-pressure curve changed at FRC, ERV was small (0.36 +/- 0.03 ml), and RV was determined by complete airway closure. Thus the mechanisms determining FRC are unusual and include an influence of airway closure.

Negative pressure ventilation decreases inflammation and lung edema during normothermic ex-vivo lung perfusion

2018 ◽  
Vol 37 (4) ◽  
pp. 520-530 ◽  
Author(s):  
Nader S. Aboelnazar ◽  
Sayed Himmat ◽  
Sanaz Hatami ◽  
Christopher W. White ◽  
Mohamad S. Burhani ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Ex Vivo ◽  
Lung Perfusion ◽  
Lung Edema ◽  
Ex Vivo Lung Perfusion ◽  
Negative Pressure Ventilation

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.

Perfusion fixation of lungs for structure-function analysis: credits and limitations

1982 ◽  
Vol 53 (2) ◽  
pp. 528-533 ◽  
Author(s):  
H. Bachofen ◽  
A. Ammann ◽  
D. Wangensteen ◽  
E. R. Weibel
Keyword(s):  
Osmium Tetroxide ◽  
Function Analysis ◽  
Transpulmonary Pressure ◽  
Uranyl Acetate ◽  
Vascular Perfusion ◽  
Lung Weight ◽  
Physiological Variables ◽  
Isotonic Buffer ◽  
Perfusion Fixation

The quality of tissue preservation in lungs fixed by vascular perfusion has been reevaluated. Excised rabbit lungs inflated to 60% of total lung capacity were perfused (zone III conditions) with different but widely used fixatives. The effects of the perfusates on pertinent physiological variables have been assessed by a continuous monitoring, the effects on the pulmonary microstructure by qualitative and morphometric analysis of electron micrographs. Important results include the following. 1) Perfusions with isotonic glutaraldehyde at flow rates within the physiological range produce large increases of perfusion pressure and lung weight that reflect intracellular, interstitial, and intra-alveolar edema. 2) No edema occurs if glutaraldehyde is added to isotonic buffer solutions (total osmolarity 510 mosM). 3) Glutaraldehyde as sole perfusate does not fully eliminate the retractive force of lung tissue. Upon release of transpulmonary pressure the lungs retract by an indeterminable amount. 4) Satisfactory results can be obtained by sequential perfusion with osmium tetroxide and uranyl acetate or glutaraldehyde (510 mosM) followed by osmium tetroxide and uranyl acetate. The latter combination yields optimal preparations to study the alveolar and capillary architecture but causes a hyperosmotic volume loss of lung cells (cell shrinkage).

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