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Pulmonary Surfactant (pulmonary + surfactant)
Selected AbstractsPhospholipase A2 is present in meconium and inhibits the activity of pulmonary surfactant: an in vitro studyACTA PAEDIATRICA, Issue 4 2001AJJ Schrama Atelectasis, a major contributor to pulmonary dysfunction in meconium aspiration syndrome (MAS), is produced by bronchiolar obstruction and surfactant inactivation. It has been shown that substances in meconium, e.g. fatty acids, inhibit surfactant activity. However, the role of the enzyme phospholipase A2 (PLA2), which hydrolyses surfactant in adult respiratory distress syndrome (ARDS), has not yet been studied. Our objective was to investigate whether PLA2 is present in meconium and inhibits pulmonary surfactant activity in vitro. Therefore, the presence of PLA2 activity in meconium, collected from 10 newborns, was measured by the formation of lysophosphatidylcholine after incubation of meconium with radioactively labelled dipalmitoylphosphati-dylcholine. Meconium was fractionated by Sephadex G-100 column chromatography and the fractions were assayed for PLA2 activity. Also, their effect on the surface tension of surfactant (Curosurf) was measured using a pulsating bubble surfactometer (PBS). PLA2 activity was present in all meconium samples. Addition of meconium to surfactant significantly increased surface tension (mean ± SD: 17 ± 1.6 mN/m to 24.3 ± 6.7 mN/m, p= 0.0001) and only the addition of the PLA2 containing fraction from meconium to surfactant also significantly increased surface tension (mean 1.7 ± 1.6mN/m to 19.0 ± 3.58 mN/m, p < 0.0001). Conclusion: PLA2 is present in meconium and inhibits the activity of pulmonary surfactant in vitro. Therefore, PLA2 in meconium may contribute to surfactant inactivation and alveolar ateectasis in MAS. [source] Overcoming surfactant inhibition with polymersACTA PAEDIATRICA, Issue 12 2000PA Dargaville Inhibition of the function of pulmonary surfactant in the alveolar space is an important element of the pathophysiology of many lung diseases, including meconium aspiration syndrome, pneumonia and acute respiratory distress syndrome. The known mechanisms by which surfactant dysfunction occurs are (a) competitive inhibition of phospholipid entry into the surface monolayer (e.g. by plasma proteins), and (b) infiltration and destabilization of the surface film by extraneous lipids (e.g. meconium-derived free fatty acids). Recent data suggest that addition of non-ionic polymers such as dextrano and polyethylene glycol to surfactant mixtures may significantly improve resistance to inhibition. Polymers have been found to neutralize the effects of several different inhibitors, and can produce near-complete restoration of surfactant function. The anti-inhibitory properties of polymers, and their possible role as an adjunct to surfactant therapy, deserve further exploration. [source] The biology of vernix caseosaINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 5 2006S. B. Hoath Synopsis The biology and physical properties of the uniquely human skin cream ,vernix caseosa' are discussed. This material coats the foetal skin surface during the last trimester of gestation and provides multiple beneficial functions for the foetus and newborn infant. Vernix has a complex structure similar to stratum corneum but lacks lipid lamellae and is more plastic due to the absence of desmosomal constraints. In utero, vernix is made in part by foetal sebaceous glands, interacts with pulmonary surfactant, detaches into the amniotic fluid, and is swallowed by the foetus. At the time of birth, vernix has a remarkably constant water content approximating 80%. Postnatally, vernix is simultaneously a cleanser, a moisturizer, an anti-infective, and an anti-oxidant. Vernix facilitates acid mantle development and supports normal bacterial colonization. Its hydrated cellular structure and unusual lipid composition provide a ,best' solution for the needs of the foetus and newborn, not least of which is the attraction of caregivers. Vernix is an important natural biomaterial of potential interest to cosmetic scientists, and other disciplines involved in product development and therapies targeting the complex interface between the stratum corneum and a changing terrestrial environment. Résumé La biologie et les propriétés physiques de la crème de peau exclusivement humaine ,Vernix caseosa « sont discutées. Ce matériau couvre la surface de la peau foetale pendant le dernier trimestre de gestation et remplit des fonctions avantageuses multiples pour le foetus et le nouveau-né. Le Vernix a une structure complexe semblable au stratum corneum, mais manque de lamelles lipidiques et est plus plastique en raison de l'absence de contraintes desmosomales. In utero, le Vernix est constitué en partie par des glandes sébacées foetales, il interagit avec le surfactant pulmonaire, il se détache dans le liquide amniotique et est avalé par le foetus. Au moment de la naissance, le Vernix a une teneur remarquablement constante en eau de l'ordre de 80%. Après la naissance, le Vernix devient simultanément un produit de lavage, un produit hydratant, un anti-infectieux et un anti-oxydant. Le Vernix facilite le développement du manteau acide et soutient la colonisation bactérienne normale. Sa structure cellulaire hydratée et sa composition en lipide inhabituelle en font ,une des meilleures » solutions pour les besoins du foetus et du nouveau-né, à laquelle le personnel soignant n'attache pas la moindre importance. Le Vernix est un biomatériau naturel important potentiellement intéressant pour les scientifiques cosméticiens et pour les autres disciplines impliquées dans le développement de produits et de thérapies visant l'interface complexe entre le stratum corneum et un environnement terrestre changeant. [source] The effect of elevated dietary cholesterol on pulmonary surfactant function in adolescent micePEDIATRIC PULMONOLOGY, Issue 5 2008K.C. McCrae PhD Abstract It has been established that phospholipids and cholesterol interact in films of pulmonary surfactant (PS). Generally it is thought that phospholipids increase film stability whereas cholesterol increases film fluidity. To study this further, we modified dietary cholesterol in mice which received either standard rodent lacking cholesterol (sd), or high cholesterol (2%) diet (hc) for 1 month. Phospholipid stability was investigated by a capillary surfactometer (CS), which measures airflow resistance and patency. PS was collected by bronchiolar lavage and centrifuged to obtain the surface-active film (SAF). Results showed that the hc-SAF had significantly more cholesterol than sd-SAF. CS analyses at 37°C showed no significance differences in airflow resistance between hc-SAF and sd-SAF. However, at 37°C, sd-SAF showed greater ability to maintain patency compared to hc-SAF, whereas at 42°C hc-SAF showed patency ability similar to sd-SAF. The results suggested that increased cholesterol in hc-SAF induced less stability in the SAF possibly due to cholesterol's fluidizing effect on phospholipids at physiological temperatures. Pediatr Pulmonol. 2008; 43:426,434. © 2008 Wiley-Liss, Inc. [source] Contribution of pulmonary surfactant with inhaled nitric oxide for treatment of pulmonary hypertensionPEDIATRICS INTERNATIONAL, Issue 5 2006SATOSHI KUSUDA Abstract Background: Combined therapy of inhaled nitric oxide (iNO) with pulmonary surfactant replacement was reported to improve oxygenation in patients or animal models of persistent pulmonary hypertension of the newborn with pulmonary surfactant deficiency lung. To evaluate the potential of iNO for the treatment of persistent pulmonary hypertension of the newborn, pulmonary arterial pressure (PAP) was measured during iNO before and after pulmonary surfactant replacement in an animal model of pulmonary hypertension with surfactant deficiency. Methods: Seven newborn piglets were injected with L-nitro-arginine-methylester to produce an animal model of pulmonary hypertension. After PAP increased, iNO (30 p.p.m.) was introduced. Then iNO was stopped, and animals were subjected to lung lavage with saline. After recording the effect of iNO, all animals then received exogenous pulmonary surfactant installation. After surfactant treatment, iNO was again introduced. Results: Pulmonary arterial pressure and systemic arterial pressure were increased significantly by >30% after infusion of L-nitro-arginine-methylester. During iNO only PAP was reduced significantly. Respiratory system compliance decreased significantly after lung lavage, and increased significantly after pulmonary surfactant replacement with concomitant increase of PaO2. In contrast, significant reduction of PAP with iNO before and after pulmonary surfactant replacement were also observed. The reduction ratios of PAP under each condition were 75.2 ± 7.4%, 81.3 ± 3.1%, and 79.1 ± 5.3%, respectively (not significant among conditions). Conclusion: These results suggest that iNO is still a potent pulmonary arterial vasodilator even under pulmonary surfactant deficiency in an animal model of pulmonary hypertension. [source] Effect of some fractions of alveolar surfactant (phospholipids and SP-A) on the bactericidal activity of different antimicrobials against some respiratory pathogensCLINICAL MICROBIOLOGY AND INFECTION, Issue 3 2001A. Ferrara Objectives To investigate the effects of physiologic concentrations, at alveolar level, of some fractions of pulmonary surfactant (phospholipids and SP-A) on the bactericidal activity of different antimicrobials against some respiratory pathogens. Methods The antimicrobial agents cefdinir, sparfloxacin, clarithromycin, teicoplanin, cefepime, ciprofloxacin, netilmicin and tobramycin, depending on their specific activity, were investigated against Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Klebsiella pneumoniae and Pseudomonas aeruginosa. Killing curves were carried out with antimicrobials at 0.5 and 2 MIC, SP-A at 1 and 5 mg/L and phospholipids at 50 mg/L. Results Time-kill experiments showed that while SP-A never modified the activity of antimicrobials, phospholipids exerted, in some cases, a weak antagonistic effect. Among antibacterials and pathogens investigated, phospholipids were able to decrease the rate of killing of cefepime and ciprofloxacin only on P. aeruginosa, both at 0.5 and at 2 MIC, with an increase of about 1 log in CFU. The combination of SP-A and phospholipids never modified the effect observed in the presence of lipids alone. Conclusions The paucity of data only allow us to observe that the examined antibiotics do not have substantially reduced activity against respiratory pathogens studied in the presence of physiologic concentrations of some fractions of surfactant. Cefepime alone already exerted a small effect, and ciprofloxacin at 2 MIC, even in the presence of phospholipids, retained its bactericidal activity. [source] | ||||||||||