Alveolar surfactant

Bernhard W, Haslam PL, Floras J (2004) From birds to humans new concepts on airways relative to alveolar surfactant. Am J Respir Cell Mol Biol 30(1 ) 6—11... 

No studies were located regarding absorption in humans or animals after inhalation exposure to 2,3-benzofuran. The partitioning of 2,3-benzofuran between particulate matter and synthetic alveolar surfactant in vitro was reported to depend upon the chemical nature of the particles (Sehnert and Risby 1988). Synthetic lung surfactant was able to dissolve 2,3-benzofuran adsorbed to particles with few active sites, but not 2,3-benzofuran adsorbed to particles with many active sites (Sehnert and Risby 1988). These data indicate that inhalation of particles containing 2,3-benzofuran would result in some absorption, depending on the nature of the particles. 

Sehnert SS, Risby TH. 1988. Chromatographic modeling of the release of particle-adsorbed molecules into synthetic alveolar surfactant. Environ Health Perspect 78 185-195. 

V(C) dependence has been studied for various surfactants such as NP20, 22-oxyethylated dodecyl alcohol, individual phospholipids and their natural mixture (amniotic fluid), lipoproteins, alveolar surfactants, therapeutic surfactants, etc. [e.g. 332,382,383-388]. For all of them this dependence is very steep. Such a course of the IV(C) curve is also... 

The alveolar surface represents a thin liquid film formed at the interface between the alveolar gas phase and a liquid hypophase covering the epithelium. This film is stabilised by the alveolar surfactant (AS), consisting mainly of phospholipids and proteins. AS plays an important role in alveolar stabilisation in the process of breathing. It is known that AS components exist as individual molecules and as various lipid and protein/lipid micellar structures present in the so-called hypophase and, according to some researchers, form a continuous lipid monolayer at the water/air interface [e.g. 1-4]. 

Positive airway pressure ventilation some experts recommend using positive pressure ventilation during the early, asymptomatic phase following phosgene exposure to prevent pulmonary edema. While positive pressure ventilation may reduce fluid accumulation, stabilize the intra-alveolar surfactant film and suppress arteriovenous shunts, many asymptomatic patients will find the treatment unacceptable (34). In addition, resources for providing prophylactic positive pressure ventilation may not be available in a mass-casualty situation. 

Lysosomes isolated from type II cells of male New Zealand White rabbits injected intratracheally with [ H]dipalmitoylphosphatidylcholine and C C]l,2-dihexadecyl-s -glycero-3-phosphocholine are the primary catabolic organelle for alveolar surfactant dipalmitoylphosphatidylcholine following reuptake by type II cells in vivo (Rider et al. 2000). 

Keywords Alveolar surfactant Curosurf Pendant drop method Surface tension... 

The lung alveolar surfactant (AS) is a complex lipid-protein mixture, essential for the normal respiratory activity [1-4]. The main AS function in vivo is to reduce the alveolar surface tension (y, mN/m) and to provide alveolar stability [5,6], The absence of a mature AS in the lungs is the main reasmi for the development of neonatal respiratory distress syndrome (NRDS) that often has a lethal outcome [7]. 

In order to determine the infants lung maturity and the necessity of surfactant therapy it is of great importance to substantiate the functionality of the alveolar surfactant, derived via invasive techniques [13], Several techniques and models have been largely used to investigate inteifacial physicochemical properties in vitro and to assess clinical efficiency of ES in vivo the Langmuir monolayer technique in combination with Wilhelmy plate method for surface tension measurements and black foam film method for determination of the ability of ES for stable film formation [14]. The pendant drop method combined with the Axisym-metric Drop Shape Analysis (ADSA) has been also used for similar purposes [4,15-18]. 

The findings presented in this note represent a physicochemical proof in vitro of the efficiency of the Curosurf treatment in vivo. On the other hand, they demonstrate the applicability of the pendant drop ADSA, which requires a minimal amount of tracheal aspirate, as a fast, informative and useful technique for in-time alveolar surfactant diagnostics. 

Exposure to organic solvents is only rarely a cause of toxic pneumonitis. However, acute exposure to very high concentrations of solvent vapours in confined spaces (e.g. in chemical tanks) maybe a cause of chemical pneumonitis and pulmonary oedema, often in victims who have been unconscious. Pneumonia and respiratory distress syndrome caused by loss of alveolar surfactant may also result from the aspiration of intentionally (e.g. by fire eaters ) or unintentionally (e.g. from siphoning petrol) ingested solvents or fuels. 

It appears that a substantial part of the airway surfactant is derived from the alveolar region, but there is also evidence for local production of surfactant. Widdicombe (41) reviewed the possible sources and potential biological role of tracheal surfactants. He concluded that the trachea contains a complex mixture of lipids, including surface-active phospholipids not characteristic of alveolar surfactant. Experiments (60) have shown that nonciliated cells of the bronchioles produce surface-active material and that these cells are involved in ion and water transport. Other studies (43) demonstrated phospholipids in secretory cells of airway submucosal glands, suggeshng local produchon of phospholipids in the... 

Gil J. Histological preservation and ultrastructure of alveolar surfactant. Annu Rev Physiol 1985 47 753-763. 

Slomiany et al. (45) reported the lipid and protein composition in tracheobronchial secretions from normal individuals and patients with cystic fibrosis. In the normal bronehial secretions, the total phospholipid was only about half as mueh as has been reported for normal alveolar surfactant (46). The largest differ-enees were in the amounts of lysophosphatidylcholine, 29.5 versus 0.4%, sphingomyelin, 15.8 versus 3.7%, and phosphatidylethanolamine, 12.4 versus 2.6%, respectively. The differences in the surfactant composition between alveolar and airway surfaetant may be due to the addition of mucus from goblet cells and submucosal mucous glands (47), and the contribution of Clara cells (48). 

In eontrast with alveolar surfactant, the source of airway surfactant is less clear (49). Since surfactant material is presumed to leave the tracheal surface by mucociliary transport, the surfactant film has to be replenished by local secretion or from the alveolar region. The two options for the origin of airway surfactant are not mutually exclusive, and it is likely that airway surfactant is derived from both alveolar and local sources. 

The surface tension of the tracheal wall in the normal rat, guinea pig, sheep, and horse is approximately 32-33 mN/m, substantially more than the plateau surface tension (23-25 mN/m) of alveolar surfactant extracts from mammalian lungs. These data are consistent with recent studies in the pig, using relatively pure extracts of tracheal fluid, that have shown that the surface tension properties of tracheal fluid are considerably less than those of BAL fluid (44). 

Ultrastructural studies of airway mucus and alveolar surfactant have been compromised by difficulties of preservation. By conventional aqueous fixation methods, the extracellular fluid lining is dissolved in the fixative more quickly than it can be stabilized. These techniques consist of either instilling the aqueous fixatives through the airways or by immersing small sections of tissue directly into the solution. This process causes the surface film to break up and to be washed away. Better preservation of the surface film was achieved by Weibel and Gil... 

Alveolar lining fluid (98,150-152) and airway mucus (153-155) also contain potent antioxidants, including catalase, superoxide dismutase, peroxidases, and glutathione. These enzymes are physically associated with airway and alveolar surfactant and may serve to protect surfactant from oxidative injury. 

Loss of alveolar surfactant activity is likely to have pathophysiological consequences. These might include an increase in the work of breathing, owing to focal or widespread atelectasis (222) augmentation of pulmonary edema, consequent to a reduction in interstitial hydrostatic pressure (223) and increased susceptibility to infection, owing to loss of the antibacterial properties of surfactant (97). Because many of the adverse effects of surfactant deficiency can be reversed... 

Seeger W, Lepper H, Wolf HRD, Neuhof H. Alteration of alveolar surfactant function after exposure to oxidative stress and to oxygenated and native arachidonic acid in vitro. Biochim Biophys Acta 1985 835 58-67. 

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