Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

RDS is the major cause of morbidity and mortality in preterm infants. Hochheim first noted the pathologic appearance of the lungs with RDS in 1903, which included alveolar collapse associated with dilatation of the alveolar ducts and terminal bronchioles. This important finding now can be best explained by the newer model of pulmonary micromechanics proposed by Weibel and Bachofen. In this model, alveoli are not individual structures, but subunits of the alveolar duct system. The alveolar stability requires particular properties of both the fibrous skeleton and the alveolar surfactant film. With increasing surface forces resulting from surfactant deficiency, the alveolar volumes and surface areas decrease, more septal segments are folded up between the adjacent ducts, thereby widening the duct system and terminal bronchioles. In this situation, the shear forces triggered by mechanical ventilation cause damage of the terminal airways with increased permeability of plasma proteins into the airspaces, which tends to aggravate alveolar instability further. Exogenous surfactant replacement produced excellent results which decreased the pulmonary complications of RDS significantly with no adverse effects. In the not too distant future this therapy will be regularly practiced in NICU.
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PMID:[Newer pathophysiologic considerations and treatment of neonatal respiratory distress syndrome (RDS)]. 307 25

The most well characterized function of pulmonary surfactant is its ability to reduce surface tension at the alveolar air-liquid interface, thereby preventing lung collapse. However, several lines of evidence suggest that surfactant may also have 'non-surfactant' functions: specific components of surfactant (proteins and phospholipids) may interact with different alveolar cells, inhaled particles and micro-organisms modulating pulmonary host defence systems. SP-A, the most abundant surfactant protein, binds to alveolar macrophages via a specific surface receptor with high affinity [128]. Such binding effects the release of reactive oxygen species from resident alveolar macrophages if SP-A is properly presented to the target cell. SP-A also stimulates chemotaxis of alveolar macrophages [142], and serves as an opsonin in the phagocytosis of herpes simplex virus [161] Candida tropicalis [138] and various bacteria [137]. In addition, SP-A enhances the uptake of particles by monocytes and culture-derived macrophages [140] and improves bacterial killing. SP-D, another hydrophobic surfactant-associated protein, might interact with alveolar macrophages as well, stimulating the release of oxygen radicals [148], while for the hydrophilic surfactant proteins SP-B and SP-C no macrophage interactions have been described so far. SP-A and SP-D are members of the so-called 'collectins', pattern recognition molecules involved in first line defence. While some surfactant proteins appear to stimulate certain macrophage defence functions, surfactant phospholipids seem to inhibit those of lymphocytes. Suppressed lymphocyte functions include lymphoproliferation in response to mitogens and alloantigens, B cell immunoglobulin production and natural killer cell cytotoxicity. Concerning surfactant's phospholipid composition phosphatidylglycerol is more suppressive than phosphatidylcholine on a molar basis [38]. Bovine surfactant has an immunosuppressive effect on the development of hypersensitivity pneumonitis in a guinea pig model [150]. Despite these interesting observations, several important questions concerning the interactions of surfactant components with pulmonary host defence systems remain unanswered. Sufficient host defence in the lungs works through various humoral-cellular systems in conjunction with the specific anatomy of the airways and the gas exchange surface--how does the surfactant system fit into this network? Surfactant and alveolar cells are both altered during lung injury--is there a relationship between alveolar cells from RDS patients and the endogenous surfactant isolated from such patients? How does exogenous surfactant as used for substitution therapy modulate the defence system of the host? Some of those artificial surfactants have been shown to inhibit the endotoxin-alveolar macrophages, PMNs and monocytes including IL-1, IL-6 and TNF [139,152].(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Host defence capacities of pulmonary surfactant: evidence for 'non-surfactant' functions of the surfactant system. 782 30

The effects of calcium, in the form of calcium chloride, at concentrations of 5 and 20 mM, were studied on the surface properties of physiologic relevance to specialised biomaterials which replace lung surfactant in Respiratory Distress Syndrome. The dynamic surface pressure, re-spreading ratio, compressibility, hysteresis area and recruitment index of pure films of the main phospholipids of pulmonary surfactant namely dipalmitoyl phosphatidylcholine, phosphatidylglycerol, phosphatidylethanolamine and of binary mixed films of these phospholipids in the ratio of 2:3 were studied both in the presence and absence of calcium by in vitro analysis using a Wilhelmy balance. Surface excess films, of each of the surfactant systems, with initial concentration 15 A2 molecule were compressed at the rate of 50 seconds/cycle past collapse till a compression ratio of 4:1. The presence of 5 mM calcium caused a significant decrease in compressibility (p < 0.05 Mann-Whitney U test) of all the surfactant monolayer films. No further benefit was obtained by adding 20 mM calcium over that of 5 mM calcium. A significant beneficial effect of calcium (p < 0.05 Mann-Whitney U test) on film stability was observed when analysing the materials in a pulsating bubble surfactometer, in which liposomal suspensions of 1% concentration in the presence of 5 mM calcium were pulsated at a high frequency of 40 cycles per minute, corresponding to the respiratory frequency of neonates. The ultrastructure of the liposomal suspensions were also studied using cryogenic scanning electron microscopy and longitudinal micro-tubular structures were found on addition of 5 mM calcium, which could have resulted in the improved performance of the exogenous surfactants with respect to compressibility and stability.
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PMID:Effect of calcium on the surface properties of phospholipid monolayers with respect to surfactant formulations in respiratory distress syndrome. 1128 78