Introduction: Ventilator-induced Lung Injury: Not Only Air Leaks Ventilation-induced Pulmonary Edema and Related Findings: A Historical Perspective Ventilation-induced Pulmonary Edema: Hydrostatic or Permeability Edema? Experimental Evidence for Increased Vascular Transmural Pressure Evidence for Alterations in Alveolar–Capillary Permeability Contributions of the Static and Dynamic Lung Volume Components to Ventilator-induced Edema High-volume Lung Edema Low Lung Volume Injury Effects of High-volume Ventilation on Abnormal Lungs Effects of High-volume Ventilation on Injured Lungs Interaction between Severe Alveolar Flooding and Mechanical Ventilation Effects of Resting the Lung on Ventilator-induced Lung Injury Possible Mechanisms of Ventilation-induced Lung Injury Mechanisms of Increased Vascular Transmural Pressure Mechanisms of Altered Permeability Clinical Relevance

Ventilator-induced lung injury: lessons from experimental studies.

Recent observations suggest that a low surface tension may be an important attribute of the lining of the air passages of the lung.1-4The purpose of this paper is to present evidence that the material responsible for such a low surface tension is absent in the lungs of infants under 1,100-1,200 gm. and in those dying with hyaline membrane disease. The role of this deficiency in the pathogenesis of the disease is considered. Surface tension operates so as to minimize the area of the surface. In the lungs, where the internal surface (the alveolar lining) is curved concave to the airway, the tendency of the surface to become smaller promotes collapse. Although the forces not only of surface tension but also of the elastic tissue tend to collapse the lungs, their behavior differs in one important respect. When the lung contains only a small volume of air, the elastic

Surface properties in relation to atelectasis and hyaline membrane disease.

MEAD, JERE, TAMOTSU TAKISHIMA, AND DAVID LEITH. Stress distribution in lungs: a model of pulmonary elasticity. J. Appl. Physiol. 28(5) : 596-608. 1970.Although lungs are exposed to transpulmonary pressure, the air spaces within are distended solely by forces applied from surrounding tissues. By relating these forces to the areas on which they operate, we derive the effective pressure distending air spaces. In uniformly expanded lungs this pressure probably approximates transpulmonary pressure. In nonuniformly expanded lungs the effective distending pressure differs from transpulmonary pressure, and in the appropriate sign to reduce the nonuniformity. This interdependence of air-space distention bears on a number of aspects of pulmonary function, including the size of air spaces which may be expanded from the gas-free state, the static and dynamic stability of air spaces, the dryness of air spaces, the forces distending airways and blood vessels within lungs, and the distribution of pulmonary edema. The principal function of the mechanical interdependence would appear to be to support uniform expansion of air spaces. The principal functional risk that it entails is increase in capillary transmural pressure in regions which become subjected to abnormally high outward-acting stress.

Stress distribution in lungs: a model of pulmonary elasticity

Because the lungs function as the body's gas-exchange organ, they are inevitably exposed to air that is contaminated with pathogens, allergens and pollutants. Host-defence mechanisms within the lungs must facilitate clearance of inhaled pathogens and particles while minimizing an inflammatory response that could damage the thin, delicate gas-exchanging epithelium. Pulmonary surfactant is a complex of lipids and proteins that enhances pathogen clearance and regulates adaptive and innate immune-cell functions. In this article, I review the structure and functions of the surfactant proteins SP-A and SP-D in regulating host immune defence and in modulating inflammatory responses.

Immunoregulatory functions of surfactant proteins.

Pulmonary surfactant: functions and molecular composition

IN acute lung œdema in the rabbit, fluid a ad foam are found in the trachea. This foam has an altogether peculiar property, in that it is unaffected by silicone anti-foams; these rapidly destroy the foams produced by shaking œdema fluid or blood serum with air. Equally stable foam is found in the bronchi of an animal the respiratory movements of which have been paralysed and into the trachea of which a mixture of oxygen and ammonia gas has been insufflated for one or two hours; similar foams are obtained from healthy lung by cutting and squeezing under water, or after introduction of saline into the trachea. The stability of such foams is due to an insoluble surface layer on the bubbles; this layer can be attacked by pancreatin or by trypsin.

Properties, function and origin of the alveolar lining layer.

The properties of foam and bubbles arising in the lung have been studied, and evidence has been obtained as to the nature of the alveolar lining. In acute lung oedema, whether accompanied by respiratory movement or not, foam is found in the trachea; it is unaffected by chemical anti-foams, which rapidly destroy the foam formed by shaking oedema fluid with air. A method for obtaining similar foam from excised lung is described. In air-saturated water, bubbles 40 µ in diameter, obtained from the lung, may be stable for hours, while ordinary bubbles of this size contract and disappear in a few minutes under the influence of surface tension. From observations of these and also from measurements of sessile bubbles, it is shown that their surface tension may be less than 0.06 dyn/cm. The 9stability ratio’ of such bubbles is defined. They are stabilized by a layer of insoluble protein about 50 A thick, and it is shown that this can only have had its origin as the original lining of the alveoli of the lungs. If the sharply curved alveolar surface had a surface tension as great as that of blood serum, there would be produced a negative pressure which would draw a transudate from the blood into the alveoli. The lining layer prevents this by reducing the surface tension to nearly zero. From observations on bubbles obtained from the lung under various conditions, it is shown that the lining layer is produced by surface adsorption from a substance (the lung lining substance) present as a jolly or slime lining the small air spaces. In the guinea-pig it develops only late in foetal life. Its peculiar surface properties are not present in blood or in tracheal mucus; it is therefore a specialized secretion and not a transudate from the blood. Methods for preparing atelectatic lung in vitro and for obtaining a solution of the lung lining substance are described. From gastric mucin, which has properties somewhat similar to those of the lung lining substance, a foam highly resistant to anti-foams has been prepared. The possible origin and pathological significance of the lung lining are discussed.

Pattle Re

Papers

Properties, function and origin of the alveolar lining layer.

Properties, function, and origin of the alveolar lining layer