Статті в журналах: "Pulmonary surfactant"

1

van Golde, LMG, JJ Batenburg, and B. Robertson. "The Pulmonary Surfactant System." Physiology 9, no. 1 (February 1, 1994): 13–20. http://dx.doi.org/10.1152/physiologyonline.1994.9.1.13.

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The pulmonary surfactant system includes specific proteins involved in the regulation of surfactant secretion and recycling, conversion of secreted lamellar bodies to tubular myelin, film adsorption, and stimulation of alveolar macrophages. Hydrophobic proteins are essential for the rapid physiological action of exogenous surfactants currently used in clinical practice.

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2

Ramanathan, Rangasamy. "Surfactants in the Management of Respiratory Distress Syndrome in Extremely Premature Infants." Journal of Pediatric Pharmacology and Therapeutics 11, no. 3 (July 1, 2006): 132–44. http://dx.doi.org/10.5863/1551-6776-11.3.132.

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Respiratory distress syndrome (RDS) is primarily due to decreased production of pulmonary surfactant, and it is associated with significant neonatal morbidity and mortality. Exogenous pulmonary surfactant therapy is currently the treatment of choice for RDS, as it demonstrates the best clinical and economic outcomes. Studies confirm the benefits of surfactant therapy to include reductions in mortality, pneumothorax, and pulmonary interstitial emphysema, as well as improvements in oxygenation and an increased rate of survival without bronchopulmonary dysplasia. Phospholipids (PL) and surfactant-associated proteins (SP) play key roles in the physiological activity of surfactant. Different types of natural and synthetic surfactant preparations are currently available. To date, natural surfactants demonstrate superior outcomes compared to the synthetic surfactants, at least during the acute phase of RDS. This disparity is often attributed to biochemical differences including the presence of surfactant-associated proteins in natural products that are not found in the currently available synthetic surfactants. Comparative trials of the natural surfactants strive to establish the precise differences in clinical outcomes among the different preparations. As new surfactants become available, it is important to evaluate them relative to the known benefits of the previously existing surfactants. In order to elucidate the role of surfactant therapy in the management of RDS, it is important to review surfactant biochemistry, pharmacology, and outcomes from randomized clinical trials.

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3

Bernhard, Wolfgang, Andreas Gebert, Gertrud Vieten, Gunnar A. Rau, Jens M. Hohlfeld, Anthony D. Postle, and Joachim Freihorst. "Pulmonary surfactant in birds: coping with surface tension in a tubular lung." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 1 (July 1, 2001): R327—R337. http://dx.doi.org/10.1152/ajpregu.2001.281.1.r327.

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As birds have tubular lungs that do not contain alveoli, avian surfactant predominantly functions to maintain airflow in tubes rather than to prevent alveolar collapse. Consequently, we have evaluated structural, biochemical, and functional parameters of avian surfactant as a model for airway surfactant in the mammalian lung. Surfactant was isolated from duck, chicken, and pig lung lavage fluid by differential centrifugation. Electron microscopy revealed a uniform surfactant layer within the air capillaries of the bird lungs, and there was no tubular myelin in purified avian surfactants. Phosphatidylcholine molecular species of the various surfactants were measured by HPLC. Compared with pig surfactant, both bird surfactants were enriched in dipalmitoylphosphatidylcholine, the principle surface tension-lowering agent in surfactant, and depleted in palmitoylmyristoylphosphatidylcholine, the other disaturated phosphatidylcholine of mammalian surfactant. Surfactant protein (SP)-A was determined by immunoblot analysis, and SP-B and SP-C were determined by gel-filtration HPLC. Neither SP-A nor SP-C was detectable in either bird surfactant, but both preparations of surfactant contained SP-B. Surface tension function was determined using both the pulsating bubble surfactometer (PBS) and capillary surfactometer (CS). Under dynamic cycling conditions, where pig surfactant readily reached minimal surface tension values below 5 mN/m, neither avian surfactant reached values below 15 mN/m within 10 pulsations. However, maximal surface tension of avian surfactant was lower than that of porcine surfactant, and all surfactants were equally efficient in the CS. We conclude that a surfactant composed primarily of dipalmitoylphosphatidylcholine and SP-B is adequate to maintain patency of the air capillaries of the bird lung.

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4

PUTMAN, Esther, Lambert A. J. M. CREUWELS, Lambert M. G. van GOLDE, and Henk P. HAAGSMAN. "Surface properties, morphology and protein composition of pulmonary surfactant subtypes." Biochemical Journal 320, no. 2 (December 1, 1996): 599–605. http://dx.doi.org/10.1042/bj3200599.

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Separation of surfactant subtypes is now commonly used as a parameter in assessing the amount of active compared with inactive material in various models of lung injury. The protein content, morphology and surface activity were determined of the heavy and light subtype isolated by differential centrifugation. Here we report the presence of surfactant proteins B and C in the heavy subtype but not in the light subtype. Adsorption studies revealed that separation of fast adsorbing bronchoalveolar lavage resulted in slowly adsorbing heavy and light subtypes. Surfactant, reconstituted from heavy and light fractions, did not show a high adsorption rate. It is concluded that the isolation procedures might result in a loss of fast adsorbing surfactant structures. Surface area cycling was used as a model in vitro for the extracellular surfactant metabolism. The heavy subtype is converted into the light subtype during conversion. Conversion performed with resuspended heavy subtype revealed the generation of a disparate subtype. Furthermore it was found that the conversion was dependent on preparation and handling of the samples before cycling. Finally, adsorption studies at low surfactant concentrations revealed a delayed adsorption of lipid-extracted surfactants compared with natural surfactants. These observations emphasize the importance of the (surfactant-associated protein A-dependent) structural organization of surfactant lipids in the adsorption process.

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5

Dobbs, L. G. "Pulmonary Surfactant." Annual Review of Medicine 40, no. 1 (February 1989): 431–46. http://dx.doi.org/10.1146/annurev.me.40.020189.002243.

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6

Johansson, Jan, Magnus Gustafsson, Marie Palmblad, Shahparak Zaltash, Bengt Robertson, and Tore Curstedt. "Pulmonary Surfactant." BioDrugs 11, no. 2 (1999): 71–77. http://dx.doi.org/10.2165/00063030-199911020-00001.

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7

Nguyen, Thuy N., Stephanie M. Cunsolo, Peter Gal, and J. Laurence Ransom. "Infasurf and Curosurf: Theoretical and Practical Considerations with New Surfactants." Journal of Pediatric Pharmacology and Therapeutics 8, no. 2 (April 1, 2003): 97–114. http://dx.doi.org/10.5863/1551-6776-8.2.97.

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Type II pneumocytes, normally responsible for surfactant production and release, are insufficiently formed and differentiated in the premature infant born before 34 weeks' gestation. Without an adequate amount of pulmonary surfactant, alveolar surface tension increases, leading to collapse and decreased lung compliance. Pulmonary surfactants are naturally occurring substances made of lipids and proteins. They lower surface tension at the interface between the air in the lungs, specifically at the alveoli, and the blood in the capillaries. This review examines the relative benefits of the two most recently marketed surfactants, calfactan (Infasurf) and poractant alfa (Curosurf).

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8

Rosenberg, O. A. "Pulmonary Surfactant Preparations and Surfactant Therapy for ARDS in Surgical Intensive Care (a Literature Review)." Creative surgery and oncology 9, no. 1 (April 25, 2019): 50–65. http://dx.doi.org/10.24060/2076-3093-2019-9-1-50-65.

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Introduction. Despite the fact that clinical studies of pulmonary surfactants conducted over many years have demonstrated their efficacy for the treatment of acute respiratory distress syndrome (ARDS) which led to their approval for use inRussia andBelarus, only a few similar positive results have been achieved in other countries. This calls for an extensive literature review for intensive care professionals.Materials and methods. Using the data from 87 papers this review covers the composition, properties, methods of administration and delivery strategies of surfactant in the treatment and prevention of ARDS in patients with sepsis, severe complex injuries, inhalation injuries and a range of complications associated with thoracic and cardiovascular surgical procedures, massive blood transfusions, severe obstetric pathologies and the A/H1N1 pneumonia.Results. The early administration of natural pulmonary surfactants within 24 hours following the onset of ARDS as a part of the ARDS combination treatment or prevention drives down the time on mechanical ventilation to six days or shorter, prevents ventilator-associated and hospital-acquired pneumonias, bringing the respiratory failure mortality rate down to 15–20%.Discussion. Offering the first attempt to discuss the causes of failure of Phase III multicenter clinical trials outsideRussia andBelarus, this review outlines recent developments in synthetic and powdered pulmonary surfactant preparations.Conclusion. Pulmonary surfactants are highly effective as a part of complex therapy in ARDS treatment and prevention, resulting in two to four fold drop in ARDS mortality rate. The timing of administration is seen as the key factor of the efficacy of surfactant therapy, explaining the differences in clinical trials results from different countries.

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9

Nishijima, Koji, Ken-ichi Shukunami, Hideo Yoshinari, Jin Takahashi, Hideyuki Maeda, Hitoshi Takagi, and Fumikazu Kotsuji. "Interactions among pulmonary surfactant, vernix caseosa, and intestinal enterocytes: intra-amniotic administration of fluorescently liposomes to pregnant rabbits." American Journal of Physiology-Lung Cellular and Molecular Physiology 303, no. 3 (August 1, 2012): L208—L214. http://dx.doi.org/10.1152/ajplung.00081.2011.

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Although vernix caseosa is known to be a natural biofilm at birth, human pulmonary surfactant commences to remove the vernix from fetal skin into the amniotic fluid at gestational week 34, i.e., well before delivery. To explain this paradox, we first produced two types of fluorescently labeled liposomes displaying morphology similar to that of pulmonary surfactant and vernix caseosa complexes. We then continuously administered these liposomes into the amniotic fluid space of pregnant rabbits. In addition, we produced pulmonary surfactant and vernix caseosa complexes and administered them into the amniotic fluid space of pregnant rabbits. The intra-amniotic infused fluorescently labeled liposomes were absorbed into the fetal intestinal epithelium. However, the liposomes were not transported to the livers of fetal rabbits. We also revealed that continuous administration of micelles derived from pulmonary surfactants and vernix caseosa protected the small intestine of the rabbit fetus from damage due to surgical intervention. Our results indicate that pulmonary surfactant and vernix caseosa complexes in swallowed amniotic fluid might locally influence fetal intestinal enterocytes. Although the present studies are primarily observational and further studies are needed, our findings elucidate the physiological interactions among pulmonary, dermal-epidermal, and gastrointestinal developmental processes.

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10

Wright, Jo Rae, and Samuel Hawgood. "Pulmonary Surfactant Metabolism." Clinics in Chest Medicine 10, no. 1 (March 1989): 83–93. http://dx.doi.org/10.1016/s0272-5231(21)00606-7.

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11

Wood, Alastair J. J., and Alan H. Jobe. "Pulmonary Surfactant Therapy." New England Journal of Medicine 328, no. 12 (March 25, 1993): 861–68. http://dx.doi.org/10.1056/nejm199303253281208.

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12

LACAZE-MASMONTEIL, THIERRY. "Pulmonary surfactant proteins." Critical Care Medicine 21, Supplement (September 1993): S376—S378. http://dx.doi.org/10.1097/00003246-199309001-00048.

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13

Kuroki, Y., and D. R. Voelker. "Pulmonary surfactant proteins." Journal of Biological Chemistry 269, no. 42 (October 1994): 25943–46. http://dx.doi.org/10.1016/s0021-9258(18)47138-4.

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14

SHANNON, DANIEL C. "Pulmonary Surfactant System." Anesthesiology 62, no. 2 (February 1, 1985): 216. http://dx.doi.org/10.1097/00000542-198502000-00040.

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15

&NA;. "Pulmonary surfactant genetics." Advances in Anatomic Pathology 5, no. 2 (March 1998): 118. http://dx.doi.org/10.1097/00125480-199803000-00023.

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16

Aliouat, EM, R. Escamilla, C. Cariven, C. Vieu, C. Mullet, E. Dei-Cas, and MC Prevost. "Surfactant changes during experimental pneumocystosis are related to Pneumocystis development." European Respiratory Journal 11, no. 3 (March 1, 1998): 542–47. http://dx.doi.org/10.1183/09031936.98.11030542.

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Pneumocystosis-related surfactant changes have been reported in both humans and corticosteroid-treated experimental hosts. As corticosteroids induce an increase in pulmonary surfactant, some findings could be considered as controversial. The aim of this study was to investigate whether the surfactant composition changes during experimental pneumocystosis were related to the Pneumocystis development. In this work two corticosteroid-untreated animal models were used: rabbits, which develop spontaneous pneumocystosis at weaning; and severe combined immunodeficiency mice, which were intranasally inoculated with Pneumocystis carinii. Surfactant phospholipid and protein content was explored by bronchoalveolar lavage. The in vitro effect of surfactant on P. carinii growth was also explored. In the two models, the surfactant phospholipid/protein ratio was significantly increased, whereas parasite rates were low. This ratio decreases with the slope increase of the parasite growth curve. These early surfactant changes suggested that Pneumocystis proliferation requires alveolar lining fluid changes, and that normal surfactant is not suitable for parasite development. In this way, in vitro experiments presented here have revealed an inhibitory effect of synthetic or seminatural surfactants on the P. carinii growth. Further studies are needed to determine how Pneumocystis induces the reported early modifications of the surfactant, and why the parasite development is inhibited by pulmonary surfactant.

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17

Rahaman, Sk Mehebub, Budhadeb Chowdhury, Animesh Acharjee, Bula Singh, and Bidyut Saha. "Surfactant-based therapy against COVID-19: A review." Tenside Surfactants Detergents 58, no. 6 (November 1, 2021): 410–15. http://dx.doi.org/10.1515/tsd-2021-2382.

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Abstract The coronavirus disease 2019 (COVID-19) has led to serious health and economic damage to all over the world, and it still remains unstoppable. The SARS-CoV-2, by using its S-glycoprotein, binds with an angiotensin-converting enzyme 2 receptor, mostly present in alveolar epithelial type II cells. Eventually pulmonary surfactant depletion occurs. The pulmonary surfactant is necessary for maintaining the natural immunity as well as the surface tension reduction within the lung alveoli during the expiration. Its insufficiency results in the reduction of blood oxygenation, poor pulmonary regeneration, lung fibrosis, and finally the respiratory system collapses. Exogenous surfactants have previously shown great promise in the treatment of infant respiratory distress syndrome, and they may also aid in the healing of damaged alveolar cells and the prevention of respiratory failure. Surfactant based therapy has been advised for the prevention of COVID-19, and the trials have begun around the world. Furthermore, greater research on the timing, dose, and the distribution of surfactant to the COVID-19 patients is required before this technique can be implemented in clinical practice.

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18

Kobayashi, T., W. Z. Li, K. Tashiro, R. Takahashi, Y. Waseda, K. Yamamoto, and Y. Suzuki. "Disparity between tidal and static volumes of immature lungs treated with reconstituted surfactants." Journal of Applied Physiology 80, no. 1 (January 1, 1996): 62–68. http://dx.doi.org/10.1152/jappl.1996.80.1.62.

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We biologically assessed functions of several reconstituted surfactants with the same minimum surface tension (2-3 mN/m) as “complete” porcine pulmonary surfactant (natural surfactant) but with longer surface adsorption times. Administration of natural surfactant (adsorption time 0.29 s) into the lungs of surfactant-deficient immature rabbits brought a tidal volume of 16.1 +/- 4.4 (SD) ml/kg during mechanical ventilation with 40 breaths/min and 20 cmH2O insufflation pressure. In static pressure-volume recordings, these animals showed a lung volume of 62.4 +/- 9.7 ml/kg at 30 cmH2O airway pressure and maintained 55% of this volume when the pressure decreased to 5 cmH2O. With two reconstituted surfactants consisting of synthetic lipids or isolated lipids from porcine lungs plus surfactant-associated hydrophobic proteins (adsorption times 0.57 and 0.78 s, respectively), tidal volumes were < 38% of that with natural surfactant (P < 0.05), but static pressure-volume recordings were not different. Care is therefore needed in estimating the in vivo function of surfactant preparations from minimum surface tension or static pressure-volume measurements.

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19

Walther, Frans J., Monik Gupta, Michael M. Lipp, Holly Chan, John Krzewick, Larry M. Gordon, and Alan J. Waring. "Aerosol delivery of dry powder synthetic lung surfactant to surfactant-deficient rabbits and preterm lambs on non-invasive respiratory support." Gates Open Research 3 (January 14, 2019): 6. http://dx.doi.org/10.12688/gatesopenres.12899.1.

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Background: The development of synthetic lung surfactant for preterm infants has focused on peptide analogues of native surfactant proteins B and C (SP-B and SP-C). Non-invasive respiratory support with nasal continuous positive airway pressure (nCPAP) may benefit from synthetic surfactant for aerosol delivery. Methods: A total of three dry powder (DP) surfactants, consisting of phospholipids and the SP-B analogue Super Mini-B (SMB), and one negative control DP surfactant without SMB, were produced with the Acorda Therapeutics ARCUS® Pulmonary Dry Powder Technology. Structure of the DP surfactants was compared with FTIR spectroscopy, in vitro surface activity with captive bubble surfactometry, and in vivo activity in surfactant-deficient adult rabbits and preterm lambs. In the animal experiments, intratracheal (IT) aerosol delivery was compared with surfactant aerosolization during nCPAP support. Surfactant dosage was 100 mg/kg of lipids and aerosolization was performed using a low flow inhaler. Results: FTIR spectra of the three DP surfactants each showed secondary structures compatible with peptide folding as an α-helix hairpin, similar to that previously noted for surface-active SMB in other lipids. The DP surfactants with SMB demonstrated in vitro surface activity <1 mN/m. Oxygenation and lung function increased quickly after IT aerosolization of DP surfactant in both surfactant-deficient rabbits and preterm lambs, similar to improvements seen with clinical surfactant. The response to nCPAP aerosol delivery of DP surfactant was about 50% of IT aerosol delivery, but could be boosted with a second dose in the preterm lambs. Conclusions: Aerosol delivery of active DP synthetic surfactant during non-invasive respiratory support with nCPAP significantly improved oxygenation and lung function in surfactant-deficient animals and this response could be enhanced by giving a second dose. Aerosol delivery of DP synthetic lung surfactant has potential for clinical applications.

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20

Walther, Frans J., Monik Gupta, Michael M. Lipp, Holly Chan, John Krzewick, Larry M. Gordon, and Alan J. Waring. "Aerosol delivery of dry powder synthetic lung surfactant to surfactant-deficient rabbits and preterm lambs on non-invasive respiratory support." Gates Open Research 3 (March 14, 2019): 6. http://dx.doi.org/10.12688/gatesopenres.12899.2.

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Background: The development of synthetic lung surfactant for preterm infants has focused on peptide analogues of native surfactant proteins B and C (SP-B and SP-C). Non-invasive respiratory support with nasal continuous positive airway pressure (nCPAP) may benefit from synthetic surfactant for aerosol delivery. Methods: A total of three dry powder (DP) surfactants, consisting of phospholipids and the SP-B analogue Super Mini-B (SMB), and one negative control DP surfactant without SMB, were produced with the Acorda Therapeutics ARCUS® Pulmonary Dry Powder Technology. Structure of the DP surfactants was compared with FTIR spectroscopy, in vitro surface activity with captive bubble surfactometry, and in vivo activity in surfactant-deficient adult rabbits and preterm lambs. In the animal experiments, intratracheal (IT) aerosol delivery was compared with surfactant aerosolization during nCPAP support. Surfactant dosage was 100 mg/kg of lipids and aerosolization was performed using a low flow inhaler. Results: FTIR spectra of the three DP surfactants each showed secondary structures compatible with peptide folding as an α-helix hairpin, similar to that previously noted for surface-active SMB in other lipids. The DP surfactants with SMB demonstrated in vitro surface activity <1 mN/m. Oxygenation and lung function increased quickly after IT aerosolization of DP surfactant in both surfactant-deficient rabbits and preterm lambs, similar to improvements seen with clinical surfactant. The response to nCPAP aerosol delivery of DP surfactant was about 50% of IT aerosol delivery, but could be boosted with a second dose in the preterm lambs. Conclusions: Aerosol delivery of DP synthetic surfactant during non-invasive respiratory support with nCPAP significantly improved oxygenation and lung function in surfactant-deficient animals and this response could be enhanced by giving a second dose. Aerosol delivery of DP synthetic lung surfactant has potential for clinical applications.

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21

Soll, Roger F., and Jerold F. Lucey. "Surfactant Replacement Therapy." Pediatrics In Review 12, no. 9 (March 1, 1991): 261–67. http://dx.doi.org/10.1542/pir.12.9.261.

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Despite medical and technological advances, respiratory distress syndrome (RDS) remains a major cause of morbidity and mortality in premature infants. Thirty years have passed since Avery and Mead demonstrated that infants dying of RDS were deficient in pulmonary surfactant. In those three decades, advances in our understanding of the composition, function, and metabolism of pulmonary surfactant have finally led to clinical trials of surfactant replacement therapy in thousands of premature infants. This article reviews the current status of surfactant replacement therapy. BACKGROUND Pulmonary surfactant is essential for normal lung function. Surfactant forms a film at the alveolar surface, which prevents the lung from collapsing at the end of expiration. Surfactant may have other functions as well, including the prevention of pulmonary edema, the prevention of infection, and the prevention of lung injury from toxic substances, such as oxygen (Table 1) CHEMICAL MAKEUP The chemical makeup of pulmonary surfactant has been well defined (Table 2). Lipids are the major component, comprising up to 80% to 90% of surfactant by weight. The majority of the lipids in pulmonary surfactant are highly polar phospholipids, predominantly phosphatidylcholine. Three proteins associated with surfactant have been these surfactant proteins may play a critical role in surfactant function by improving the adsorption of surfactant at the alveolar surface and by aiding in surfactant re-uptake and metabolism.

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22

Elssner, Andreas, Gertraud Mazur, and Claus Vogelmeier. "Inhibition of factor XIIIa-mediated incorporation of fibronectin into fibrin by pulmonary surfactant." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 4 (April 1, 1999): L625—L630. http://dx.doi.org/10.1152/ajplung.1999.276.4.l625.

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Intra-alveolar deposition of exudated plasma proteins is a hallmark of acute and chronic inflammatory lung diseases. In particular, fibrin and fibronectin may provide a primary matrix for fibrotic lung remodeling in the alveolar compartment. The present study was undertaken to explore the effect of two surfactant preparations on the incorporation of fibronectin into fibrin. We observed that surfactant phospholipids are associated with insoluble fibrin, factor XIIIa-cross-linked fibrin, and cross-linked fibrin with incorporated fibronectin. Factor XIIIa-mediated binding of fibronectin to fibrin was noticeably altered in the presence of surfactant. Coincubation with two different commercially available surfactants but not with dipalmitoylphosphatidylcholine alone resulted in a reduction of fibronectin incorporation into fibrin clots by approximately one-third. This effect was not dependent on the calcium concentration. We conclude that 1) factor XIIIa-cross-linked fibrin-fibronectin is able to incorporate surfactant phospholipids in amounts comparable to fibrin clots without fibronectin and 2) the binding of fibronectin to fibrin is partially inhibited in the presence of pulmonary surfactant.

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23

Sherman, M. P., J. B. D'Ambola, E. E. Aeberhard, and C. T. Barrett. "Surfactant therapy of newborn rabbits impairs lung macrophage bactericidal activity." Journal of Applied Physiology 65, no. 1 (July 1, 1988): 137–45. http://dx.doi.org/10.1152/jappl.1988.65.1.137.

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Because in vitro studies indicate that pulmonary alveolar macrophages (PAM's) filled with phospholipid vesicles have depressed microbicidal capacity, we tested the intrapulmonary bactericidal activity of newborn PAM's after surfactant treatment. Term newborn rabbits received intratracheally either homologous surfactant or one of two artificial phospholipid vesicle preparations followed by pulmonary aerosol infection with group B streptococci (GBS). Four hours after lung infection, phagocytic killing of GBS was reduced by 70-90% in animals treated with the homologous and one of the artificial surfactants compared with untreated animals or animals that received intrapulmonary injections of the surfactant vehicle (P less than 0.02). The other artificial phospholipid preparation decreased intrapulmonary inactivation of GBS by 30-40% compared with the controls. The phospholipid vesicles in the three preparations were avidly ingested and processed by newborn PAM's. The diminished in vivo killing of GBS was not attributed to decreased viability or phagocytic behavior of the PAM's toward GBS. The bactericidal defect that was evident in the newborn PAM's appeared related to the uptake of large phospholipid vesicles in the preparations rather than to the phospholipid content of the surfactants themselves. When in vitro conditions that stimulated the alveolar environment were used, the natural surfactant preparation promoted GBS proliferation, whereas the artificial preparations did not. Our findings indicate that surfactant administration reduces the bactericidal activity of neonatal PAM's. We conclude that additional investigations are needed to ascertain the effect of surfactant replacement therapy on lost defenses of the lung.

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24

Kosim, M. Sholeh. "Use of surfactant in neonatal intensive care units." Paediatrica Indonesiana 45, no. 6 (October 13, 2016): 233. http://dx.doi.org/10.14238/pi45.6.2005.233-40.

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Surfactant is currently an important therapyfor newborns in neonatal intensive care units(NICUs) with respiratory problems,specifically respiratory distress syndrome(RDS). Surfactant was initially used in 1959, after itwas recognized for maintaining lung inflation at lowtranspulmonary pressures. Avery and Mead in Jobereported that saline extracts from the lungs ofpreterm infants with RDS lacked the low surfacetension characteristics of pulmonary surfactant.Subsequently, in 1980, clinical potential of surfactanttherapy for RDS was demonstrated by Fujiwara et al,reported in Jobe, in the use of surfactant preparedfrom an organic solvent extracted from bovine lung(Surfactant TA). Small randomized controlled trials(RCTs) in 1985, which tested surfactants preparedfrom bovine alveolar-lavage or human amniotic fluid,demonstrated significant decrease in pneumothoraxand death rates. Subsequent multi-center trialsdemonstrated decreased death rates andcomplications of RDS; although still investigational,its use begun in 1989. A synthetic surfactant wasapproved for the treatment of the syndrome in theUnited States in 1990, and an animal surfactant wasapproved in 1991. These surfactants represent a newclass of drug developed specifically for preterminfants.

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25

Gemci, Tevfik, Valery Ponyavin, Richard Collins, Timothy E. Corcoran, Suvash C. Saha, and Mohammad S. Islam. "CFD Study of Dry Pulmonary Surfactant Aerosols Deposition in Upper 17 Generations of Human Respiratory Tract." Atmosphere 13, no. 5 (May 2, 2022): 726. http://dx.doi.org/10.3390/atmos13050726.

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The efficient generation of high concentrations of fine-particle, pure surfactant aerosols provides the possibility of new, rapid, and effective treatment modalities for Acute Respiratory Distress Syndrome (ARDS). SUPRAER-CATM is a patented technology by Kaer BiotherapeuticsTM, which is a new class of efficient aerosol drug generation and delivery system using Compressor Air (CA). SUPRAER-CA is capable of aerosolizing relatively viscous solutions or suspensions of proteins and surfactants and of delivering them as pure fine particle dry aerosols. In this Computational Fluid Dynamics (CFD) study, we select a number of sites within the upper 17 generations of the human respiratory tract for calculation of the deposition of dry pulmonary surfactant aerosol particles. We predict the percentage of inhaled dry pulmonary surfactant aerosol arriving from the respiratory bronchioles to the terminal alveolar sacs. The dry pulmonary surfactant aerosols, with a Mass Median Aerodynamic Diameter (MMAD) of 2.6 µm and standard deviation of 1.9 µm, are injected into the respiratory tract at a dry surfactant aerosol flow rate of 163 mg/min to be used in the CFD study at an air inhalation flow rate of 44 L/min. This CFD study in the upper 17th generation of a male adult lung has shown computationally that the penetration fraction (PF) is approximately 25% for the inhaled surfactant aerosols. In conclusion, an ARDS patient might receive approximately one gram of inspired dry surfactant aerosol during an administration period of one hour as a possible means of further inflating partly collapsed alveoli.

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26

Gross, N. J. "Pulmonary surfactant: unanswered questions." Thorax 50, no. 4 (April 1, 1995): 325–27. http://dx.doi.org/10.1136/thx.50.4.325.

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27

Rider, Evelyn. "Metabolism of Pulmonary Surfactant." Seminars in Respiratory and Critical Care Medicine 16, no. 01 (January 1995): 17–28. http://dx.doi.org/10.1055/s-2007-1009812.

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28

Caminiti, Stephen P., and Stephen L. Young. "The Pulmonary Surfactant System." Hospital Practice 26, no. 1 (January 15, 1990): 87–100. http://dx.doi.org/10.1080/21548331.1991.11704128.

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29

Chroneos, Zissis C., Krishna Midde, Zvjezdana Sever-Chroneos, and Chinnaswamy Jagannath. "Pulmonary surfactant and tuberculosis." Tuberculosis 89 (December 2009): S10—S14. http://dx.doi.org/10.1016/s1472-9792(09)70005-8.

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30

Weaver, Timothy E. "Pulmonary surfactant-associated proteins." General Pharmacology: The Vascular System 19, no. 3 (January 1988): 361–68. http://dx.doi.org/10.1016/0306-3623(88)90029-8.

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31

Liu, Lin, and Quanmin Deng. "Profound Effect of Pulmonary Surfactant on the Treatment of Preterm Infants with Respiratory Distress Syndrome." Contrast Media & Molecular Imaging 2022 (October 3, 2022): 1–10. http://dx.doi.org/10.1155/2022/4166994.

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Анотація:

Inherited diseases caused by dysfunction of pulmonary surfactant metabolism or surfactant dysfunction have recently been considered the underlying causes of neonatal and pediatric respiratory diseases. Respiratory distress syndrome in premature infants is a common respiratory disease in pediatrics. It is caused by underdeveloped lungs in infants and a lack of active substances on the surface of the alveoli, which leads to insufficiency of lung function, which can lead to difficulty breathing, increased heart rate, facial bruising, and more. Neonatal Respiratory Distress Syndrome is a very dangerous disease with a high mortality rate and a great threat to children’s lives and health. Therefore, enough attention and treatment should be caused in clinical practice. Natural pulmonary surfactant (PS) has achieved positive effects in the treatment of neonatal respiratory distress syndrome (RDS), reducing neonatal mortality, the application of mechanical ventilation, and the occurrence of late complications. To further explore the role of pulmonary surfactants in the treatment of neonatal respiratory distress syndrome, to analyze the best time to use PS to prevent RDS, this paper has selected premature infants with RDS received by the neonatal department of a hospital in a province from March 2019 to October 2020 to compare the efficacy of pulmonary surfactant (PS) in preterm infants with respiratory distress syndrome (RDS). The experiment has found that the average mechanical ventilation time (5.1 d) and oxygen therapy time (7.3 d) in the early group are shorter than the average mechanical ventilation time (6.4 d) and oxygen therapy time (10.6 d) in the late group. It has been demonstrated that early administration of pulmonary surfactant (PS) therapy is of great help in improving respiratory distress syndrome in premature infants.

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32

Wright, J. R. "Clearance and recycling of pulmonary surfactant." American Journal of Physiology-Lung Cellular and Molecular Physiology 259, no. 2 (August 1, 1990): L1—L12. http://dx.doi.org/10.1152/ajplung.1990.259.2.l1.

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In a steady state the rate of secretion of pulmonary surfactant lipids and proteins into the alveolar airspace must be balanced by the rate of removal. Several potential pathways for clearance have been identified including uptake by alveolar type II cells, which also synthesize and secrete surfactant components, uptake by other epithelial cells, and internalization by alveolar macrophages. A small amount of surfactant moves up the airways and through the epithelium-endothelium barrier into the blood. Some of the surfactant lipids and proteins that are cleared from the alveolar airspace appear to be “recycled” in that they appear in the lamellar body, a surfactant secretory granule found in the type II cell. Some surfactant lipids are degraded, probably intracellularly, and the degradation products are reutilized to synthesize new lipids. Several factors have been shown to affect internalization by the type II cell and/or alveolar clearance including the surfactant proteins, lipids, and known stimuli of surfactant secretion. Surfactant proteins may be involved in regulating pool size by modulating both secretion rates and uptake rates, possibly by a receptor-mediated process, although such receptors have not yet been identified or isolated. Clearance of surfactant lipids from the alveolar airspace is more rapid than clearance from the whole lung, and these two processes may be regulated by different factors. Elucidation of the factors that fine tune the balance between synthesis, secretion, and clearance of the lipid and protein components of surfactant awaits further investigation

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33

Seeger, W., C. Grube, A. Gunther, and R. Schmidt. "Surfactant inhibition by plasma proteins: differential sensitivity of various surfactant preparations." European Respiratory Journal 6, no. 7 (July 1, 1993): 971–77. http://dx.doi.org/10.1183/09031936.93.06070971.

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Leakage of plasma proteins into the alveolar space may inhibit surfactant function. We compared the surface properties and the sensitivity to inhibitory proteins of different organic solvent surfactant extracts and a synthetic surfactant. Experiments were performed in the pulsating bubble surfactometer, with surfactant concentrations ranging between 0.1 and 2 mg.ml-1. Inhibition profiles towards fibrinogen, albumin and haemoglobin were obtained from calf lung surfactant extracts (CLSE), Alveofact, Curosurf and Survanta (all used in clinical, replacement studies in respiratory distress syndrome (RDS) and of an apoprotein-based synthetic phospholipid mixture (PLM-C/B; DPPC:PG:PA = 68.5:22.5:9, supplemented with 2% wt/wt non-palmitoylated human recombinant SP-C and 1% t/wt natural bovine SP-B). In the absence of inhibitory proteins, all surfactants exhibited dose-dependent rapid adsorption (rank order of relative efficacy PLM-C/B = CLSE > Alveofact > Curosurf > Survanta). Minimal surface tension was reduced to near zero values under dynamic compression (rank order PLM-C/B > CLSE > Alveofact = Curosurf) and to approximately 4 mN.m-1 (Survanta). Curosurf and Survanta were dose-dependently inhibited by fibrinogen > haemoglobin > albumin, with far-reaching loss of surface activity at protein-surfactant ratios above 1:1. In contrast, CLSE and Alveofact were only moderately inhibited by fibrinogen, and were not affected by haemoglobin and albumin, up to protein-surfactant ratios of 2:1. PLM-C/B exhibited resistance to fibrinogen, intermediate sensitivity to albumin, and was severely inhibited by haemoglobin. We conclude that various natural surfactant extracts and an apoprotein-based synthetic surfactant mixture markedly differ in their sensitivity to inhibitory plasma proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

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Homer, Robert J., Tao Zheng, Geoff Chupp, Susan He, Zhou Zhu, Quingshen Chen, Bing Ma, et al. "Pulmonary type II cell hypertrophy and pulmonary lipoproteinosis are features of chronic IL-13 exposure." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 1 (July 1, 2002): L52—L59. http://dx.doi.org/10.1152/ajplung.00438.2001.

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Interleukin (IL)-13, a key mediator of Th2-mediated immunity, contributes to the pathogenesis of asthma and other pulmonary diseases via its ability to generate fibrosis, mucus metaplasia, eosinophilic inflammation, and airway hyperresponsiveness. In these studies, we compared surfactant accumulation in wild-type mice and mice in which IL-13 was overexpressed in the lung. When compared with littermate controls, transgenic animals showed alveolar type II cell hypertrophy under light and electron microscopy. Over time, their alveoli also filled with surfactant in a pulmonary alveolar proteinosis pattern. At the same time, prominent interstitial fibrosis occurs. Bronchoalveolar lavage fluid from these mice had a three- to sixfold increase in surfactant phospholipids. Surfactant proteins (SP)-A, -B, and -C showed two- to threefold increases, whereas SP-D increased 70-fold. These results indicate that IL-13 is a potent stimulator of surfactant phospholipid and surfactant accumulation in the lung. IL-13 may therefore play a central role in the broad range of chronic pulmonary conditions in which fibrosis, type II cell hypertrophy, and surfactant accumulation occur.

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35

Rider, E. D., A. H. Jobe, M. Ikegami, and B. Sun. "Different ventilation strategies alter surfactant responses in preterm rabbits." Journal of Applied Physiology 73, no. 5 (November 1, 1992): 2089–96. http://dx.doi.org/10.1152/jappl.1992.73.5.2089.

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The effect of ventilation strategy on in vivo function of different surfactants was evaluated in preterm rabbits delivered at 27 days gestational age and ventilated with either 0 cmH2O positive end-expiratory pressure (PEEP) at tidal volumes of 10–11 ml/kg or 3 cmH2O PEEP at tidal volumes of 7–8 ml/kg after treatment with one of four different surfactants: sheep surfactant, the lipids of sheep surfactant stripped of protein (LH-20 lipid), Exosurf, and Survanta. The use of 3 cmH2O PEEP decreased pneumothoraces in all groups except for the sheep surfactant group where pneumothoraces increased (P < 0.01). Ventilatory pressures (peak pressures - PEEP) decreased more with the 3 cmH2O PEEP, low-tidal-volume ventilation strategy for Exosurf-, Survanta-, and sheep surfactant-treated rabbits (P < 0.05), whereas ventilation efficiency indexes (VEI) improved only for Survanta- and sheep surfactant-treated rabbits with 3 cmH2O PEEP (P < 0.01). Pressure-volume curves for sheep surfactant-treated rabbits were better than for all other treated groups (P < 0.01), although Exosurf and Survanta increased lung volumes above those in control rabbits (P < 0.05). The recovery of intravascular radiolabeled albumin in the lungs and alveolar washes was used as an indicator of pulmonary edema. Only Survanta and sheep surfactant decreased protein leaks in the absence of PEEP, whereas all treatments decreased labeled albumin recoveries when 3 cmH2O PEEP was used (P < 0.05). These experiments demonstrate that ventilation style will alter a number of measurements of surfactant function, and the effects differ for different surfactants.

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36

Milad, Nadia, and Mathieu C. Morissette. "Revisiting the role of pulmonary surfactant in chronic inflammatory lung diseases and environmental exposure." European Respiratory Review 30, no. 162 (December 15, 2021): 210077. http://dx.doi.org/10.1183/16000617.0077-2021.

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Pulmonary surfactant is a crucial and dynamic lung structure whose primary functions are to reduce alveolar surface tension and facilitate breathing. Though disruptions in surfactant homeostasis are typically thought of in the context of respiratory distress and premature infants, many lung diseases have been noted to have significant surfactant abnormalities. Nevertheless, preclinical and clinical studies of pulmonary disease too often overlook the potential contribution of surfactant alterations – whether in quantity, quality or composition – to disease pathogenesis and symptoms. In inflammatory lung diseases, whether these changes are cause or consequence remains a subject of debate. This review will outline 1) the importance of pulmonary surfactant in the maintenance of respiratory health, 2) the diseases associated with primary surfactant dysregulation, 3) the surfactant abnormalities observed in inflammatory pulmonary diseases and, finally, 4) the available research on the interplay between surfactant homeostasis and smoking-associated lung disease. From these published studies, we posit that changes in surfactant integrity and composition contribute more considerably to chronic inflammatory pulmonary diseases and that more work is required to determine the mechanisms underlying these alterations and their potential treatability.

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37

Orgeig, Sandra, Allan W. Smits, Christopher B. Daniels, and Jay K. Herman. "Surfactant regulates pulmonary fluid balance in reptiles." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 6 (December 1, 1997): R2013—R2021. http://dx.doi.org/10.1152/ajpregu.1997.273.6.r2013.

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Reptilian lungs are potentially susceptible to fluid disturbances because they have very high pulmonary fluid filtration rates. In mammals, pulmonary surfactant protects the lung from developing alveolar edema. Reptiles also have an order of magnitude more surfactant per square centimeter of respiratory surface area compared with mammals. We investigated the role of reptilian surfactant 1) in the entry of vascularly derived fluid into the alveolar space of the isolated perfused lizard ( Pogona vitticeps) lung and 2) in the removal of accumulated fluid from the alveolar space of the isolated perfused turtle ( Trachemys scripta) lung by both the pulmonary venous and lymphatic circulations. The flux of fluorescent (fluorescein isothiocyanate) inulin from the vasculature into the alveolar compartment increased 60% after the removal of surfactant, but capillary fluid filtration over a 10-min period was not affected. Surfactant removal decreased alveolar inulin clearance by both the pulmonary venous circulation and the pulmonary lymphatic system ∼1.5- and 3-fold, respectively. In reptiles, fluid flux from capillary to air space must occur indirectly via the interstitium. In the absence of surfactant, this may result in interstitial drying, which affects both pulmonary venous and pulmonary lymphatic clearance of alveolar fluid.

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Notter, Robert H., Rohun Gupta, Adrian L. Schwan, Zhengdong Wang, Mohanad Gh Shkoor, and Frans J. Walther. "Synthetic lung surfactants containing SP-B and SP-C peptides plus novel phospholipase-resistant lipids or glycerophospholipids." PeerJ 4 (October 27, 2016): e2635. http://dx.doi.org/10.7717/peerj.2635.

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BackgroundThis study examines the biophysical and preclinical pulmonary activity of synthetic lung surfactants containing novel phospholipase-resistant phosphonolipids or synthetic glycerophospholipids combined with Super Mini-B (S-MB) DATK and/or SP-Css ion-lock 1 peptides that replicate the functional biophysics of surfactant proteins (SP)-B and SP-C. Phospholipase-resistant phosphonolipids used in synthetic surfactants are DEPN-8 and PG-1, molecular analogs of dipalmitoyl phosphatidylcholine (DPPC) and palmitoyl-oleoyl phosphatidylglycerol (POPG), while glycerophospholipids used are active lipid components of native surfactant (DPPC:POPC:POPG 5:3:2 by weight). The objective of the work is to test whether these novel lipid/peptide synthetic surfactants have favorable preclinical activity (biophysical, pulmonary) for therapeutic use in reversing surfactant deficiency or dysfunction in lung disease or injury.MethodsSurface activity of synthetic lipid/peptide surfactants was assessedin vitroat 37 °C by measuring adsorption in a stirred subphase apparatus and dynamic surface tension lowering in pulsating and captive bubble surfactometers. Shear viscosity was measured as a function of shear rate on a Wells-Brookfield micro-viscometer.In vivopulmonary activity was determined by measuring lung function (arterial oxygenation, dynamic lung compliance) in ventilated rats and rabbits with surfactant deficiency/dysfunction induced by saline lavage to lower arterial PO2to <100 mmHg, consistent with clinical acute respiratory distress syndrome (ARDS).ResultsSynthetic surfactants containing 5:3:2 DPPC:POPC:POPG or 9:1 DEPN-8:PG-1 combined with 3% (by wt) of S-MB DATK, 3% SP-Css ion-lock 1, or 1.5% each of both peptides all adsorbed rapidly to low equilibrium surface tensions and also reduced surface tension to ≤1 mN/m under dynamic compression at 37 °C. However, dual-peptide surfactants containing 1.5% S-MB DATK + 1.5% SP-Css ion-lock 1 combined with 9:1 DEPN-8:PG-1 or 5:3:2 DPPC:POPC:POPG had the greatestin vivoactivity in improving arterial oxygenation and dynamic lung compliance in ventilated animals with ARDS. Saline dispersions of these dual-peptide synthetic surfactants were also found to have shear viscosities comparable to or below those of current animal-derived surfactant drugs, supporting their potential ease of deliverability by instillation in future clinical applications.DiscussionOur findings support the potential of dual-peptide synthetic lipid/peptide surfactants containing S-MB DATK + SP-Css ion-lock 1 for treating diseases of surfactant deficiency or dysfunction. Moreover, phospholipase-resistant dual-peptide surfactants containing DEPN-8/PG-1 may have particular applications in treating direct forms of ARDS where endogenous phospholipases are present in the lungs.

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39

Erokhin, V. V., L. N. Lepekha, M. V. Erokhina, I. V. Bocharova, A. V. Kurynina, and G. E. Onishchenko. "SELECTIVE EFFECTS OF PULMONARY SURFACTANT ON VARIOUS SUBPOPULATIONS OF ALVEOLAR MACROPHAGES IN THE MODEL OF EXPERIMENTAL TUBERCULOSIS." Annals of the Russian academy of medical sciences 67, no. 11 (November 10, 2012): 22–28. http://dx.doi.org/10.15690/vramn.v67i11.467.

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Pulmonary surfactant is necessary component for maintenance of high level of phagocytic activity of alveolar macrophages. Tuberculosis inflammation reduces the production of surfactant by type II cells and phagocytic activity of alveolar macrophages. The effects of exogenous pulmonary surfactant on the ultrastructural changes of various subpopulations of alveolar macrophages were studied by TEM-method. For investigations the bronchial alveolar lavage fluid from guinea pigs infected of M. tuberculosis and treated by isoniazid or isoniazid + exogenous pulmonary surfactant were used. It was shown that isoniazid + exogenous pulmonary surfactant normalizes the heterogeneous population of alveolar macrophages providing stimulating effects on their maturation and phagocytic activity more effectively than isoniazid therapy.

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40

Ballard, Philip L., Jeffrey D. Merrill, Rodolfo I. Godinez, Marye H. Godinez, William E. Truog, and Roberta A. Ballard. "Surfactant Protein Profile of Pulmonary Surfactant in Premature Infants." American Journal of Respiratory and Critical Care Medicine 168, no. 9 (November 2003): 1123–28. http://dx.doi.org/10.1164/rccm.200304-479oc.

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41

Beers, Michael F., Aaron Hamvas, Michael A. Moxley, Linda W. Gonzales, Susan H. Guttentag, Kola O. Solarin, William J. Longmore, Lawrence M. Nogee, and Philip L. Ballard. "Pulmonary Surfactant Metabolism in Infants Lacking Surfactant Protein B." American Journal of Respiratory Cell and Molecular Biology 22, no. 3 (March 2000): 380–91. http://dx.doi.org/10.1165/ajrcmb.22.3.3645.

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42

Whitsett, Jeffrey A. "Review: The intersection of surfactant homeostasis and innate host defense of the lung: lessons from newborn infants." Innate Immunity 16, no. 3 (March 29, 2010): 138–42. http://dx.doi.org/10.1177/1753425910366879.

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The study of pulmonary surfactant, directed towards prevention and treatment of respiratory distress syndrome in preterm infants, led to the identification of novel proteins/genes that determine the synthesis, packaging, secretion, function, and catabolism of alveolar surfactant. The surfactant proteins, SP-A, SP-B, SP-C, and SP-D, and the surfactant lipid associated transporter, ABCA3, play critical roles in surfactant homeostasis. The study of their structure and function provided insight into a system that integrates the biophysical need to reduce surface tension in the alveoli and the innate host defenses required to maintain pulmonary structure and function after birth. Alveolar homeostasis depends on the intrinsic, multifunctional structures of the surfactant-associated proteins and the shared transcriptional regulatory modules that determine both the expression of genes involved in surfactant production as well as those critical for host defense. Identification of the surfactant proteins and the elucidation of the genetic networks regulating alveolar homeostasis have provided the basis for understanding and diagnosing rare and common pulmonary disorders, including respiratory distress syndrome, inherited disorders of surfactant homeostasis, and pulmonary alveolar proteinosis.

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43

Horowitz, A. D., K. Kurak, B. Moussavian, J. A. Whitsett, S. E. Wert, W. M. Hull, J. McNanie, and M. Ikegami. "Preferential uptake of small-aggregate fraction of pulmonary surfactant in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 2 (August 1, 1997): L468—L477. http://dx.doi.org/10.1152/ajplung.1997.273.2.l468.

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Homeostasis of pulmonary surfactant requires metabolic clearance of surfactant forms with decreased surface activity. Rabbit pulmonary surfactant was labeled in vivo with rhodamine-labeled dipalmitoylphosphatidylethanolamine (R-DPPE), isolated, and fractionated into large- and small-aggregate subfractions by differential centrifugation. Endocytosis of large (LA)- and small (SA)-aggregate surfactant by a mouse lung epithelial cell line (MLE-12) was evaluated in vitro by epifluorescence microscopy. More SA than LA surfactant was taken up by MLE-12 cells. Endocytosis of SA and LA surfactant was inhibited by preincubation of the subfractions with surfactant protein A and 3.3 mM Ca2+. The difference in uptake between SA and LA surfactant was lost for reconstituted organic extracts of the subfractions. Much of the difference in uptake of SA and LA surfactant may be attributed to the greater concentration of surfactant protein A in LA surfactant.

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44

Graham, Emma, Lynda McCaig, Gloria Shui-Kei Lau, Akash Tejura, Anne Cao, Yi Y. Zuo, and Ruud Veldhuizen. "E-cigarette aerosol exposure of pulmonary surfactant impairs its surface tension reducing function." PLOS ONE 17, no. 11 (November 9, 2022): e0272475. http://dx.doi.org/10.1371/journal.pone.0272475.

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Introduction E-cigarette (EC) and vaping use continue to remain popular amongst teenage and young adult populations, despite several reports of vaping associated lung injury. One of the first compounds that EC aerosols comes into contact within the lungs during a deep inhalation is pulmonary surfactant. Impairment of surfactant’s critical surface tension reducing activity can contribute to lung dysfunction. Currently, information on how EC aerosols impacts pulmonary surfactant remains limited. We hypothesized that exposure to EC aerosol impairs the surface tension reducing ability of surfactant. Methods Bovine Lipid Extract Surfactant (BLES) was used as a model surfactant in a direct exposure syringe system. BLES (2ml) was placed in a syringe (30ml) attached to an EC. The generated aerosol was drawn into the syringe and then expelled, repeated 30 times. Biophysical analysis after exposure was completed using a constrained drop surfactometer (CDS). Results Minimum surface tensions increased significantly after exposure to the EC aerosol across 20 compression/expansion cycles. Mixing of non-aerosolized e-liquid did not result in significant changes. Variation in device used, addition of nicotine, or temperature of the aerosol had no additional effect. Two e-liquid flavours, menthol and red wedding, had further detrimental effects, resulting in significantly higher surface tension than the vehicle exposed BLES. Menthol exposed BLES has the highest minimum surface tensions across all 20 compression/expansion cycles. Alteration of surfactant properties through interaction with the produced aerosol was observed with a basic e-liquid vehicle, however additional compounds produced by added flavourings appeared to be able to increase inhibition. Conclusion EC aerosols alter surfactant function through increases in minimum surface tension. This impairment may contribute to lung dysfunction and susceptibility to further injury.

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Fisher, James H., Vladimir Sheftelyevich, Ye-Shih Ho, Suzanne Fligiel, Francis X. McCormack, Thomas R. Korfhagen, Jeffrey A. Whitsett, and Machiko Ikegami. "Pulmonary-specific expression of SP-D corrects pulmonary lipid accumulation in SP-D gene-targeted mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 2 (February 1, 2000): L365—L373. http://dx.doi.org/10.1152/ajplung.2000.278.2.l365.

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Targeted disruption of the surfactant protein (SP) D ( SP-D) gene caused a marked pulmonary lipoidosis characterized by increased alveolar lung phospholipids, demonstrating a previously unexpected role for SP-D in surfactant homeostasis. In the present study, we tested whether the local production of SP-D in the lung influenced surfactant content in SP-D-deficient [SP-D(−/−)] and SP-D wild-type [SP-D(+/+)] mice. Rat SP-D (rSP-D) was expressed under control of the human SP-C promoter, producing rSP-D, SP-D(+/+) transgenic mice. SP-D content in bronchoalveolar lavage fluid was increased 30- to 50-fold in the rSP-D, SP-D(+/+) mice compared with the SP-D(+/+) parental strain. Lung morphology, phospholipid content, and surfactant protein mRNAs were unaltered by the increased concentration of SP-D. Likewise, the production of endogenous mouse SP-D mRNA was not perturbed by the SP-D transgene. rSP-D, SP-D(+/+) mice were bred to SP-D(−/−) mice to assess whether lung-selective expression of SP-D might correct lipid homeostasis abnormalities in the SP-D(−/−) mice. Selective expression of SP-D in the respiratory epithelium had no adverse effects on lung function, correcting surfactant phospholipid content and decreasing phosphatidylcholine incorporation significantly. SP-D regulates surfactant lipid homeostasis, functioning locally to inhibit surfactant phospholipid incorporation in the lung parenchyma and maintaining alveolar phospholipid content in the alveolus. Marked increases in biologically active tissue and alveolar SP-D do not alter lung morphology, macrophage abundance or structure, or surfactant accumulation.

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Picone, Anthony, Louis A. Gatto, Gary F. Nieman, Andrew M. Paskanik, and Charles Lutz. "PULMONARY SURFACTANT FUNCTION FOLLOWING ENDOTOXIN." Shock 5, no. 4 (April 1996): 304–10. http://dx.doi.org/10.1097/00024382-199604000-00012.

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47

Bisetti, A. "Pulmonary Surfactant and Respiratory Infections." Respiration 55, no. 1 (1989): 45–48. http://dx.doi.org/10.1159/000195750.

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48

BALLARD, PHILIP L. "Hormonal Regulation of Pulmonary Surfactant." Endocrine Reviews 10, no. 2 (May 1989): 165–81. http://dx.doi.org/10.1210/edrv-10-2-165.

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49

Whitsett, Jeffrey A., Susan E. Wert, and Timothy E. Weaver. "Diseases of Pulmonary Surfactant Homeostasis." Annual Review of Pathology: Mechanisms of Disease 10, no. 1 (January 24, 2015): 371–93. http://dx.doi.org/10.1146/annurev-pathol-012513-104644.

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50

Chroneos, Zissis, Zvjezdana Sever-Chroneos, and Virginia Shepherd. "Pulmonary Surfactant: An Immunological Perspective." Cellular Physiology and Biochemistry 25, no. 001 (2010): 013–26. http://dx.doi.org/10.1159/000272047.

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