Prolonged hyperoxic exposure is associated with impaired alveolarization of the lung in both the rat and the human neonate. Elastin is currently thought to play a pivotal role in the alveolarization of the lung by providing the structural framework around which new alveoli will develop. Previous studies in both the rat and the human neonate have demonstrated a risk for proteolytic destruction of lung elastin associated with prolonged hyperoxic exposure. The present study was undertaken to determine whether continuous exposure to 100% oxygen during the period of alveolar development in the rat (Days 4 to 13) would alter lung elastin. Parenchymal lung elastic fiber length, volume density of parenchyma, mean linear intercept, and internal surface area were quantitated using morphometric techniques, and the values were compared in control, oxygen-exposed, and malnourished rat pups. Stereologic measurements indicated that total elastic fiber length was significantly greater in lungs of control pups than in lungs of either the oxygen-exposed or the malnourished pups. Examination of sections of lung tissue 20 to 30 microns thick indicated altered elastic fiber structure and numerous alveolar fenestrae only in the hyperoxic pups. The results of these studies demonstrated that hyperoxic exposure during alveolarization alters both total length and structure of lung elastic fibers and suggest that impaired lung development might be due in part to these observed changes.

A membrane model, composed of phospholipid and cholesterol, is described. The electrical resistance and hydration of this model can be controlled by manipulation of ambient ions and by current in ways strongly remiiniscent of the behavior of living cells. The behavior of the model may resemble that of the membrane component of the cell. In addition, an interdependent, lipid-protein molecular structure may exist at the cell surface.T HE ANNOUNCED TITLIE of our paper, "Further Studies on the Nature of the Excitable System in the Cell Surface," tells you the nature of the general area of our interest, but it does not tell you just what we are going to talk about. Therefore, I should like, at the outset, to give you a more precise idea of our subject. What we shall discuss first is the control of the resistance of a phospholipid-cholesterol membrane model by competition between calcium and potassium. We shall describe what we have done, what we know about mechanism, how the system responds reversibly to current flow in a way which may give us insight into the molecular underlay of excitation, and some other parallels between the model and living cells. Following this, we wish to draw attention to another matter which may, at this point, be of interest more to the chemist than to the physiologist, namely, an example of structural interdependence of lipid and protein in periaxoplasmic lamellae.But before we do this, we want to put the work in proper perspective. We have asked a question, and over a period of several years we have made a number of approaches to answering it, of which this is the third. Let ine recapitulate briefly:

A cephalin-cholesterol membrane model is described whose electrical resistance can be reversibly raised by CaCl2 or lowered by KCl or NaCl whether these ions are added to the membrane by mechanical immersion or are driven in electrically. Either KCl or NaCl acts antagonistically to CaCl2. Experiments with controlled pH indicate that the above effects depend somehow on combination of the cations with the phospholipid acidic groups. Also, they are correlated with decreased membrane hydration in CaCl2 solutions, and increased hydration in KCl or NaCl solutions. It is conjectured that cells may regulate their transsurface ion pathways and fluxes by K-Ca competition for negatively charged binding sites on plasma membrane phospholipid. It is regarded as a corollary to say that a fundamental event in excitation is displacement of membrane Ca from such a site by catelectrotonically propelled K.