Pulmonary surfactant layers accelerate O(2) diffusion through the air-water interface.

During respiration, it is accepted that oxygen diffuses passively from the lung alveolar spaces through the respiratory epithelium until reaching the pulmonary capillaries, where blood is oxygenated. It is also widely assumed that pulmonary surfactant, a lipid-protein complex secreted into alveolar spaces, has a main surface active function, essential to stabilize the air-liquid interface, reducing in this way the work of breathing. The results of the present work show that capillary water layers containing enough density of pulmonary surfactant membranes transport oxygen much faster than a pure water phase or a water layer saturated with purely lipidic membranes. Membranes reconstituted from whole pulmonary surfactant organic extract, containing all the lipids plus the hydrophobic surfactant proteins, permit also very rapid oxygen diffusion, substantially faster than achieved by membranes prepared from the surfactant lipid fraction depleted of proteins. A model is proposed suggesting that protein-promoted membrane networks formed by pulmonary surfactant might have important properties to facilitate oxygenation through the thin water layer covering the respiratory surface.

[Why are the lungs dry?]. / Weshalb ist die Lunge trocken?12.

The extremely thin blood-gas barrier, the high blood perfusion rate and the deformability of the lung required for ventilation call for safety measures in order to keep the peripheral airspaces dry. The protective factors are provided in part by the particular structural organization of the lung, in part by physiological safeguards. Amongst the structural safety factors the extremely low permeability of the alveolar epithelial cell layer, the effective drainage system of interstitial spaces, and the loose connective tissue layers which surround vessels and bronchi, and which can act as transient fluid reservoirs, should be mentioned. The physiologic safety factors include the low hemodynamic pressures in the pulmonary vessels, the high colloid-osmotic pressure of blood, the decrease in perimicrovascular colloid-osmotic pressure on increased transcapillary fluid filtration, the interstitial pressure gradient between peripheral and central parts of the lung, and the minimal mechanical forces acting on the fine lung parenchyma owing to the low surface tensions provided by alveolar surfactant. Whether the active pumping mechanism improving reabsorption of edema fluid is also operative under normal conditions has not yet been clarified.

Characterization of pulmonary cell growth parameters in a continuous perfusion microfluidic environment.

In vitro models of the alveolo-pulmonary barrier consist of microvascular endothelial cells and alveolar epithelial cells cultured on opposing sides of synthetic porous membranes. However, these simple models do not reflect the physiological microenvironment of pulmonary cells, wherein cells are exposed to a complex milieu of mechanical and soluble stimuli. In this report, we studied alveolar epithelial (A549) and microvascular endothelial (HMEC-1) cells within varying microfluidic environments as a first step towards building a microfluidic analog of the gas-exchange interface. We fabricated polydimethylsiloxane (PDMS) microdevices for parallel studies of cell growth under multiple flow rates. Cells adhered and proliferated in the microculture chambers for shear stresses up to approximately 2 x 10(-3) dynes/cm(2), corresponding to media turnover rates of approximately 53 seconds. Proliferation of these cells into confluent monolayers and expression of cell-specific markers (SP-A and CD-31) demonstrated successful pulmonary cell culture in microscale devices, a first for alveolar epithelial cells. These results represent the initial steps towards the development of microfluidic analogs of the alveolo-pulmonary barrier and tissue engineering of the lung.

Localisation of exogenous surfactants in cell membranes in the air-blood barrier: rat model.

The use of exogenous surfactants has been introduced into the therapy of patients of different ages. Much better results have been obtained in the treatment of respiratory distress syndrome with surfactants enriched with surfactant proteins. In the following study we used protein-containing surfactants (survanta and curosurf). The aim of the following study was to determine the localisation of artificial surfactants in the lung tissue. Using the Immunogold Technique, biotinylated surfactant proteins were traced in the air-blood barriers. In all lungs the exogenous surfactant was present only in some alveoli. In these parts small areas of atelectasis as well as oedema and transudate accumulation were seen. These changes were less severe after biotinylated curosurf treatment. In electron microscope studies we found surfactant elements in the air-blood barrier and other structures of the alveolar septa. Immunogold studies confirm the presence of biotynylated surfactant in the elements of the air-blood barrier.