Properties, function and origin of the alveolar lining layer.
TL;DR: 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.
Abstract: 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.
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TL;DR: This paper presents 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.
Abstract: 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
2,259 citations
TL;DR: The principal functional risk that it entails is increase in capillary transmural pressure in regions which become subjected to abnormally high outward-acting stress, and in the appropriate sign to reduce the nonuniformity.
Abstract: 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.
1,236 citations
TL;DR: The structure and functions of the surfactant proteins SP-A and SP-D in regulating host immune defence and in modulating inflammatory responses are reviewed.
Abstract: 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.
901 citations
TL;DR: It is concluded that, in spite of much effort, the authors still do not understand the basic molecular mechanisms underlying surfactant's rapid adsorption to the air-water interface.
700 citations
TL;DR: Controversy about the character of hyperplastic AE2 cells, reported to synthesise profibrotic factors, proscribes drawing a definite conclusion today.
Abstract: In 1977, Mason and Williams developed the concept of the alveolar epithelial type II (AE2) cell as a defender of the alveolus. It is well known that AE2 cells synthesise, secrete, and recycle all components of the surfactant that regulates alveolar surface tension in mammalian lungs. AE2 cells influence extracellular surfactant transformation by regulating, for example, pH and [Ca2+] of the hypophase. AE2 cells play various roles in alveolar fluid balance, coagulation/fibrinolysis, and host defence. AE2 cells proliferate, differentiate into AE1 cells, and remove apoptotic AE2 cells by phagocytosis, thus contributing to epithelial repair. AE2 cells may act as immunoregulatory cells. AE2 cells interact with resident and mobile cells, either directly by membrane contact or indirectly via cytokines/growth factors and their receptors, thus representing an integrative unit within the alveolus. Although most data support the concept, the controversy about the character of hyperplastic AE2 cells, reported to synthesise profibrotic factors, proscribes drawing a definite conclusion today.
692 citations
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