Urea permeability of alveolar membrane; hemodynamic effects of liquid in the alveolar spaces

1960 ◽  
Vol 198 (5) ◽  
pp. 1029-1031 ◽  
Author(s):  
Cecil E. Cross ◽  
P. Andre Rieben ◽  
Peter F. Salisbury

The blood flow through isolated lungs, excised or in situ, was measured while air or isotonic lavage solution was injected into and withdrawn from the lobar bronchus under variable pressures. Lavage of isolated lobes, intubated via the lobar bronchus with cuffed endotracheal tubes, was also performed in closed-chest experiments while certain hemodynamic parameters were recorded. Urea equilibration between the blood and the alveolar fluid could be expressed as an asymptotic line; the urea concentration of the alveolar fluid reached 30% and 55% of the blood urea concentration when the lavage solution remained in the alveoli for 5 and 15 minutes, respectively. Regardless of the presence or absence of liquid in the alveoli, vascular resistance in the isolated lobe was determined by airway pressure. In closed-chest experiments the hemodynamic effects of pulmonary lavage were minimal as long as low positive and negative pressures were used to inject and withdraw the lavage solution.

2018 ◽  
Vol 125 (5) ◽  
pp. 1357-1367 ◽  
Author(s):  
Tam L. Nguyen ◽  
Carrie E. Perlman

Whether alveolar liquid surface tension, T, is elevated in the acute respiratory distress syndrome (ARDS) has not been demonstrated in situ in the lungs. Neither is it known how exogenous surfactant, which has failed to treat ARDS, affects in situ T. We aim to determine T in an acid-aspiration ARDS model before and after exogenous surfactant administration. In isolated rat lungs, we combine servo-nulling pressure measurement and confocal microscopy to determine alveolar liquid T according to the Laplace relation. Administering 0.01 N (pH 1.9) HCl solution by alveolar injection or tracheal instillation, to model gastric liquid aspiration, raises T. Subsequent surfactant administration fails to normalize T. Furthermore, in normal lungs, tracheal instillation of control saline or exogenous surfactant raises T. Lavaging the trachea with saline and injecting the lavage solution into the alveolus raises T, suggesting that tracheal instillation may wash T-raising airway contents to the alveolus. Adding 0.01 N HCl or 5 mM CaCl2—either of which aggregates mucins—to tracheal lavage solution reduces or eliminates the effect of lavage solution on alveolar T. Following tracheal saline instillation, liquid suctioned directly out of alveoli through a micropipette contains mucins. Additionally, alveolar injection of gastric mucin solution raises T. We conclude that 1) tracheal liquid instillation likely washes T-raising mucins to the alveolus and 2) even exogenous surfactant that could be delivered mucin-free to the alveolus might not normalize T in acid-aspiration ARDS. NEW & NOTEWORTHY We demonstrate in situ in isolated lungs that surface tension is elevated in an acid-aspiration acute respiratory distress syndrome (ARDS) model. Following tracheal liquid instillation, also in isolated lungs, we directly sample alveolar liquid. We find that liquid instillation into normal lungs washes mucins to the alveolus, thereby raising alveolar surface tension. Furthermore, even if exogenous surfactant could be delivered mucin-free to the alveolus, exogenous surfactant might fail to normalize alveolar surface tension in acid-aspiration ARDS.


Hydrobiologia ◽  
1989 ◽  
Vol 188-189 (1) ◽  
pp. 277-283 ◽  
Author(s):  
C. Lindblad ◽  
U. Kautsky ◽  
C. André ◽  
N. Kautsky ◽  
M. Tedengren

2006 ◽  
Vol 77 (2) ◽  
pp. 023105 ◽  
Author(s):  
Simon R. Bare ◽  
George E. Mickelson ◽  
Frank S. Modica ◽  
Andrzej Z. Ringwelski ◽  
N. Yang

2012 ◽  
Vol 10 (3) ◽  
pp. 117-128 ◽  
Author(s):  
Ryan J. Bell ◽  
William B. Savidge ◽  
Strawn K. Toler ◽  
Robert H. Byrne ◽  
R. Timothy Short

2016 ◽  
Vol 206 ◽  
pp. 36-44 ◽  
Author(s):  
Marc-Antoni Goulet ◽  
Aronne Habisch ◽  
Erik Kjeang

2020 ◽  
Vol 26 (4) ◽  
pp. 34-39
Author(s):  
Boris Borisovich Yatsinyuk ◽  
◽  
Pavel Pavlovich Gavrikov ◽  
Yulia Vasilyevna Lobur

The research of an analysis of the cardiac hemodynamic effects of an acute chemical trauma with slow calcium channels blockers (verapamil) shows that the depth of disorder of cardiac hemodynamic parameters and the level and frequency of occurrence of consciousness disorder were determined in 46 patients within the period of 2007–2017 in this nosological form of acute poisoning.


1978 ◽  
Vol 76 (1) ◽  
pp. 149-165 ◽  
Author(s):  
G. M. HUGHES ◽  
G. A. VERGARA

1. Static pressure/volume curves have been determined for isolated frog lungs inflated with either air or saline. In both cases a hysteresis was present: the pressure required to produce unit change of volume being greater during inflation than deflation. 2. The pressure necessary for a given volume change was less for the saline-filled than the air-filled lungs. The difference between these curves is due to the surface tension at the air/lung interface. 3. Pressure/volume curves for air-filled lungs in situ were similar to curves for isolated lungs. However, a greater pressure was required for the same volume change during both inflation and deflation. 4. Compliance was calculated from different parts of air pressure/volume curves and gave values greater than those obtained using similar calculations for higher vertebrates. 5. These observations support other evidence for the presence of a surfactant in the lung lining of frogs in spite of the relatively large diameter of their ‘alveoli.’ The precise role of such a lining is uncertain and it is concluded that similar forces may be involved during the inflation and deflation of lungs of frogs and higher vertebrates in spite of differences in gross morphology.


1993 ◽  
Vol 74 (4) ◽  
pp. 1499-1503 ◽  
Author(s):  
W. F. Brechue ◽  
B. T. Ameredes ◽  
G. M. Andrew ◽  
W. N. Stainsby

Blood flow through the gastrocnemius-plantaris muscle of the dog in situ was increased by a pump in the arterial supply during a 30-min period of 1/s isotonic tetanic contractions. Compared with a control series of experiments with normoxemia and spontaneous flow, the pump increased flow 84%, from 1.51 +/- 0.08 to 2.78 +/- 0.15 ml.g-1.min-1. The perfusion pressure was increased from 125 to 196 mmHg. The pump hyperemia increased maximal O2 uptake (VO2) at 5 min of contractions by 31%, from 8.97 +/- 0.44 to 12.89 +/- 0.30 mumol.g-1.min-1. The extraction was decreased, and venous PO2 (PVO2) was increased. Fatigue, measured as a drop in power production from the highest level at 10 s to 30 min, was 49% during pump hyperemia and 54% in the control conditions. VO2 decreased 30% from the 5-min value to the 30-min value with pump hyperemia and 28% over the same time in the control conditions. At maximal VO2, the ratio VO2/PVO2 was increased by pump hyperemia compared with control conditions, suggesting an increased O2 diffusing conductance of the muscles. We conclude that the elevated perfusion pressure of pump hyperemia increased flow to raise maximal VO2 mainly in areas of the muscle that had restricted flow under control conditions.


1995 ◽  
Vol 79 (6) ◽  
pp. 1895-1899 ◽  
Author(s):  
W. J. Lamm ◽  
T. Obermiller ◽  
M. P. Hlastala ◽  
R. K. Albert

We previously found that up to 15% of the normal cardiac output can flow through lungs that are entirely in zone 1 and that the zone 1 pathway utilizes alveolar corner vessels. Because of the proximity of these vessels to alveoli, we hypothesized that lungs perfused under zone 1 conditions would exchange gas. We used the multiple inert gas elimination technique to assess the ventilation-perfusion (VA/Q) distribution under zones 1 and 2 in six rabbit lungs perfused with tris(hydroxymethyl)aminomethane-buffered Tyrode solution containing 1% albumin, 4% dextran, and papaverine (25 mg/l). High-frequency oscillation (tidal volume = 2.8 ml at 20 Hz, bias flow = 1 l/min) kept alveolar pressure (PA) nearly constant at 10 or 20 cmH2O. Pulmonary arterial pressure was set 2.5 cmH2O below or 5 cmH2O above PA (zones 1 and 2, respectively). Pulmonary venous pressure was kept at 0 cmH2O, with zero reference being the bottom of the lung. At PA of 10 cmH2O, flow was 64 +/- 40 and 5 +/- 3 ml/min (P < 0.05) and the mean VA/Q for perfusion was 1.1 +/- 0.4 and > 5 (P < 0.05) in zones 2 and 1, respectively. At PA of 20 cmH2O, flow was 89 +/- 36 and 22 +/- 13 ml/min (P < 0.05) and the mean VA/Q for perfusion was 0.8 +/- 0.3 and 3.7 +/- 2.4 (P < 0.05) in zones 2 and 1, respectively. Shunt averaged < 5% of total flow in all conditions. Blood flowing through vessels remaining open under zone 1 conditions 1) exchanges gas, 2) does not occur through anatomic or physiological shunts, and 3) may explain the high VA/Q seen with positive end-expiratory pressure.


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