THE PHYSIOLOGY OF LEAKY LUNGS

Abstract

This paper outlines the relationships between the structures and functions of the pulmonary epithelium and endothelium, and describes some new methods for measuring their permeability in a variety of experimental and clinical situations. Much of the work outlined in this paper is reviewed by Davies (1973), Staub (1974, 1978, 1981), Effros (1978), Staehelin and Hull (1978), Diana and Fleming (1979), and Chinard (1980). Diffuse injury of the alveolar epithelium and the pulmonary vascular endothelium may follow aspiration of gastric contents, inhalation of toxic smokes and vapours or pulmonary embolism. Similar damage may occur when the complement system is activated during haemodialysis and after trauma or infection (Hammerschmidt et al., 1980). Complement activation has also been reported after cardiopulmonary bypass (Chenoweth et al., 1981) but no correlation was found between activation and changes in arterial oxygen tension. If any injury does occur it may cause these layers to become unduly leaky to water and solute. If the injury creates holes in the epithelium large enough to leak protein then pulmonary oedema will ensue, but if the leakage is minimal and confined to small molecular weight solutes there is no clinically obvious effect. A major problem in establishing the link between a potentially damaging stimulus and this minimal pulmonary response has been the lack of an objective test to measure a deterioration in function of the vascular endothelium and, in particular, the epithelial lining of the airways and alveoli. Measurements of changes in lung mechanics or gas exchange are either non-specific or too insensitive to draw any conclusions about the functional effects of this minimal lung injury. One approach could examine the effect of lung injury on pulmonary metabolism (Said, 1979) but, so far, little is known about the