Pulmonary Blood-Gas Barrier: A Physiological Dilemma

Physiology ◽  
1993 ◽  
Vol 8 (6) ◽  
pp. 249-253
Author(s):  
JB West ◽  
O Mathieu-Costello
Keyword(s):  
Gas Exchange ◽  
Pulmonary Edema ◽  
Capillary Wall ◽  
Blood Gas ◽  
Challenging Problem ◽  
High Permeability ◽  
Gas Barrier ◽  
Permeability Pulmonary Edema ◽  
Very High

The blood-gas barrier needs to be extremely thin for gas exchange, but also immensely strong because the capillary wall stresses become very high during exercise. Failure of the barrier causes high-permeability pulmonary edema or hemorrhage. Avoiding stress failure poses a challenging problem for some animals.

Distribution of ventilation-perfusion ratios in dogs with normal and abnormal lungs

1975 ◽  
Vol 38 (6) ◽  
pp. 1099-1109 ◽  
Author(s):  
P. D. Wagner ◽  
R. B. Laravuso ◽  
E. Goldzimmer ◽  
P. F. Naumann ◽  
J. B. West
Keyword(s):  
Pulmonary Embolism ◽  
Steady State ◽  
Gas Exchange ◽  
Clinical Investigation ◽  
Inert Gas ◽  
Blood Gas ◽  
Gas Barrier ◽  
Initial Application ◽  
Arterial Po2 ◽  
Made In

We have recently described a new method for measuring distributions of ventilation-perfusion ratios (VA/Q) based on inert gas elimination. Here we report the initial application of the method in normal dogs and in dogs with pulmonary embolism, pulmonary edema, and pneumonia. Characteristic distributions appropriate to the known effects of each lesion were observed. Comparison with traditional indices of gas exchange revealed that the arterial PO2 calculated from the distributions agreed well with measured values, as did the shunts indicated by the method and by the arterial PO2 while breathing 100 per cent 02. Also the Bohr dead space closely matched the dispersion of ventilation in realtion to VA/Q. Assumptions made in the method were critically evaluated and appear justified. These include the existence of a steady state of gas exchange, an alveolar-end-capillary diffusion equilibration, and the fact that all of the observered VA/Q inequality occurs between gas exchange units in parallel. However, theoretical analysis suggests that the method can detect failure of diffusion equilbration across the blood-gas barrier should it exist. These results suggest that the method is well-suited to clinical investigation of patients with pulmonary disease.

scholarly journals Comparative physiology of the pulmonary blood-gas barrier: the unique avian solution

2009 ◽  
Vol 297 (6) ◽  
pp. R1625-R1634 ◽  
Author(s):  
John B. West
Keyword(s):  
Gas Exchange ◽  
Complete Separation ◽  
External Support ◽  
Blood Gas ◽  
Large Area ◽  
Gas Barrier ◽  
Type Iv ◽  
Pulmonary Capillaries ◽  
The Face ◽  
Flow Through

Two opposing selective pressures have shaped the evolution of the structure of the blood-gas barrier in air breathing vertebrates. The first pressure, which has been recognized for 100 years, is to facilitate diffusive gas exchange. This requires the barrier to be extremely thin and have a large area. The second pressure, which has only recently been appreciated, is to maintain the mechanical integrity of the barrier in the face of its extreme thinness. The most important tensile stress comes from the pressure within the pulmonary capillaries, which results in a hoop stress. The strength of the barrier can be attributed to the type IV collagen in the extracellular matrix. In addition, the stress is minimized in mammals and birds by complete separation of the pulmonary and systemic circulations. Remarkably, the avian barrier is about 2.5 times thinner than that in mammals and also is much more uniform in thickness. These advantages for gas exchange come about because the avian pulmonary capillaries are unique among air breathers in being mechanically supported externally in addition to the strength that comes from the structure of their walls. This external support comes from epithelial plates that are part of the air capillaries, and the support is available because the terminal air spaces in the avian lung are extremely small due to the flow-through nature of ventilation in contrast to the reciprocating pattern in mammals.

scholarly journals High permeability pulmonary edema (ARDS) during tocolytic therapy — a case report

1988 ◽  
Vol 16 (1) ◽  
pp. 45-49 ◽  
Author(s):  
Erich W. Russi ◽  
Ludwig Spaetling ◽  
Jürg Gmür ◽  
Henning Schneider
Keyword(s):  
Case Report ◽  
Pulmonary Edema ◽  
High Permeability ◽  
Permeability Pulmonary Edema

Recurrent high-permeability pulmonary edema associated with diabetic ketoacidosis

1985 ◽  
Vol 13 (1) ◽  
pp. 55-56 ◽  
Author(s):  
CHRISTIAN J. L. BRUN-BUISSON ◽  
FRANCIS BONNET ◽  
SABINE BERGERET ◽  
FRANÇOIS LEMAIRE ◽  
MAURICE RAPIN
Keyword(s):  
Pulmonary Edema ◽  
Diabetic Ketoacidosis ◽  
High Permeability ◽  
Permeability Pulmonary Edema

Vagal afferents and active upper airway closure during pulmonary edema in lambs

1999 ◽  
Vol 86 (5) ◽  
pp. 1561-1569 ◽  
Author(s):  
Véronique Diaz ◽  
Dominique Dorion ◽  
Irenej Kianicka ◽  
Patrick Létourneau ◽  
Jean-Paul Praud ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Lung Volume ◽  
Upper Airway ◽  
Vagal Afferents ◽  
Electromyographic Activity ◽  
Airway Closure ◽  
High Permeability ◽  
Lung Water ◽  
Permeability Pulmonary Edema ◽  
Insight Into

The present study was undertaken to gain further insight into the mechanisms responsible for the sustained active expiratory upper airway closure previously observed during high-permeability pulmonary edema in lambs. The experiments were conducted in nonsedated lambs, in which airflow and thyroarytenoid and inferior pharyngeal constrictor muscle electromyographic activity were recorded. We first studied the consequences of hemodynamic pulmonary edema (induced by impeding pulmonary venous return) on upper airway dynamics in five lambs; under this condition, a sustained expiratory upper airway closure consistently appeared. We then tested whether expiratory upper airway closure was related to vagal afferent activity from bronchopulmonary receptors. Five bivagotomized lambs underwent high-permeability pulmonary edema: no sustained expiratory upper airway closure was observed. Finally, we studied whether a sustained decrease in lung volume induced a sustained expiratory upper airway closure. Five lambs underwent a 250-ml pleural infusion: no sustained expiratory upper airway closure was observed. We conclude that 1) the sustained expiratory upper airway closure observed during pulmonary edema in nonsedated lambs is related to stimulation of vagal afferents by an increase in lung water and 2) a decrease in lung volume does not seem to be the causal factor.

scholarly journals Effect of high transcapillary pressures on capillary ultrastructure and permeability coefficients in dog lung

2001 ◽  
Vol 90 (2) ◽  
pp. 638-648 ◽  
Author(s):  
Michael B. Maron ◽  
Zhenxing Fu ◽  
Odile Mathieu-Costello ◽  
John B. West
Keyword(s):  
High Pressure ◽  
Pressure Group ◽  
Blood Gas ◽  
Vascular Perfusion ◽  
Gas Barrier ◽  
Lung Lobe ◽  
Lower Lung ◽  
Perfusion Fixation ◽  
Very High ◽  
Lung Lobes

To determine the correlation between ultrastructural and physiological changes in blood-gas barrier function in lungs transiently exposed to very high vascular pressures, we increased capillary transmural pressure (Ptm) of 6 canine isolated perfused left lower lung lobe preparations (high-pressure group) to 80.3 Torr for 3.8 min and then determined the capillary filtration ( K fc) and osmotic reflection (ςd) coefficients at a Ptm of 19.1 Torr in the ventilated lung lobes. This was followed by perfusion fixation of the lobes at a Ptm of 20.5 Torr for ultrastructural analysis. These data were compared with those obtained in six lobes in which Ptm was not transiently elevated before K fc, ςd, and ultrastructural evaluation. K fc was higher [0.249 ± 0.042 (SE) vs. 0.054 ± 0.009 g · min−1 · Torr−1 · 100 g−1; P < 0.01] and ςd was lower (0.52 ± 0.07 vs. 0.85 ± 0.08; P < 0.01) in the high-pressure group. In contrast, although endothelial and epithelial breaks were occasionally observed in some experiments, their incidence was not increased in the high-pressure group. These data suggest that the increased transvascular water and protein flux occurred through pathways of a size not resolvable by electron microscopy after vascular perfusion-fixation at a Ptm of 20.5 Torr.

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