• Title/Summary/Keyword: pulmonary surfactant

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The Effect on Pulmonary Indices of Surfactant Therapy for Meconium Aspiration Syndrome: Systematic Review and Meta-analysis (태변흡인증후군에서 폐표면활성제 사용이 호흡기지표에 미치는 영향에 대한 체계적 문헌고찰과 메타분석)

  • Choi, Hyun-Jin;Hahn, Seo-Kyung;Lee, Soon-Min;Kim, Han-Suk;Bae, Chong-Woo
    • Neonatal Medicine
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    • v.18 no.2
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    • pp.189-196
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    • 2011
  • Purpose: Surfactants have been used to improve oxygenation for infants with meconium aspiration syndrome (MAS). We evaluated the change of pulmonary indices after surfactant therapy for MAS through a systematic meta-analysis. Methods: Relevant randomized controlled studies (RCTs) were identified by database searches in MEDLINE, EMBASE, and CENTRAL, up to June 2011, and by additional hand searches. Data were extracted regarding pulmonary indices, such as the oxygen index and arterial alveolar oxygen gradient. Meta-analyses were separately conducted for the studies of surfactant lavage therapy and surfactant bolus therapy. The risk of bias was assessed, and clinical as well as statistical heterogeneities were also investigated. Results: Two RCTs for bolus surfactant therapy and two RCTs for surfactant lavage therapy were identified. The oxygenation index results were heterogeneous between the two studies in which bolus surfactant therapy was given, while a/A $PO_2$ showed significantly better results in the treatment group over time after use of surfactant (12 hours: WMD 0.08, 95% CI 0.04-0.12; 24 hours: WMD 0.17, 95% CI 0.06-0.28). For surfactant lavage therapy, both studies consistently suggested an interventional benefit in terms of the pulmonary indices although it did not reach statistical significance. Conclusion: Surfactant therapy appeared to improve oxygenation of infants with MAS. Since a limited number of RCTs are available in the current literature and those studies were also clinically heterogeneous in terms of illness severity and the method of surfactant use, further research is needed to gather evidence to support surfactant therapy in MAS.

Structure studies of Pulmonary Surfactant Protein B(SP-B(3,4)) by NMR Spectroscopy and Molecular Modeling

  • Kim, Yangmee;Dongha Baek;Kang, Joo-Hyun;Shin, Song-Yub;Hahm, Kyung-Soo
    • Journal of the Korean Magnetic Resonance Society
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    • v.5 no.1
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    • pp.37-45
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    • 2001
  • Synthetic pulmonary surfactants consisting of a mixture of phospholipids with synthetic peptides based on human surfactant-associated protein SP-B were prepared. These surfactants were analyzed f3r their secondary structures by circular dichroism (CD) spectroscopy and NMR spectroscopy. Two synthetic peptides (SP-B(3), SP-B(4)) combined with the phospholipid mixture displayed significant surfactant properties. The CD spectra showed that the u-helical propensities of the peptides in DPC micelles. In the NMR spectroscopy, the tertiary structures of SP-B(3) show that it has $\alpha$-helical structure from Gln5 to Arg13 in DPC micelle and SP-B(4) show that they have $\alpha$-helical structure from Gln5 to Leu12 in DPC micelle. Based on these structures, truncated peptides originated from SP-B protein, can be designed as effective synthetic surfactants for clinical use.

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Surface Activity in Various Pulmonary Diseases (각종 폐질환에서의 Pulmonary Surfactant 에 대해서)

  • Lim, Buyng-Wha;Shin, Keun-Soo;Kim, Jin-Sik
    • Journal of Chest Surgery
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    • v.5 no.1
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    • pp.1-8
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    • 1972
  • On the study of surface activity in excized lung extracts of various pulmonary diseases, following facts were concluded. 1]The minimum surface tension measured in lung extracts of tuberculous tissue surrounding cavitary lesion was 26.3dyne/cm and its stability index was 0.53. 2]Macroscopically almost normal lung tissue at a distance of tuberculous lesion in same lobe revealed 21.3 dyne/cm of minimum surface tension in extracts and its stability index showed 0.66. This low surface activity may be due to the chronic pneumonitis microscopically. 3] In the atelectatic lung which had been collapsed by chronic empyema the extracts revealed much higher minimum surface tension in 27.3 dyne/cm and its stabillry index revealed the least value of 0.47 without correlation of duration of disease. This suggests that the longstanding collapsed lung may be soon collapsed even after mechanical full expansion because of lack of surfactant.

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ANP Inhibits Surfactant Secretion from Isoproterenol Stimulated Alveolar Type II Cells

  • Lee, Young-Man
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.1
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    • pp.65-70
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    • 1997
  • In order to investigate the effect of ANP on surfactant secretion from alveolar type II cell(AT II cell) during circulatory derangement in adult respiratory distress syndrome (ARDS), the secretion of surfactant from AT II cells was evaluated in purely isolated AT II cultures from rat lungs. For the simulation of sympathetic stimulation during circulatory derangement, primary AT II cultures were incubatedwith isoproterenol and IBMX. In this isoproterenol stimulated AT II cells, ANP were added in the media for the investigation of effect of ANP on surfactant secretion from AT II cells. For the evaluation of surfactant secretion, $[^3H]-methylcholine$ was incorporated and the level of radiolabelled choline chloride secreted from the cells was determined. As previously reported, isoproterenol and IBMX stimulated surfactant secretion from AT II cells. Isoproterenol showed synergistic increase of surfactant secretion with IBMX in AT II cells. In isoproterenol stimulated AT II cells, physiological level of ANP inhibited the secretion of surfactant in primary cultures of AT II cells. On the basis of these experimental it is suggested that, in association with ciculatory change during ARDS, increased secretion of ANP by the pulmonary edema, hypoxia and congestive heart heart failure might aggravate the symptoms of ARDS by reduction of surfactant secretion from AT II cells.

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Surfactant preparations for preterm infants with respiratory distress syndrome: past, present, and future

  • Jeon, Ga Won
    • Clinical and Experimental Pediatrics
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    • v.62 no.5
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    • pp.155-161
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    • 2019
  • Following the first successful trial of surfactant replacement therapy for preterm infants with respiratory distress syndrome (RDS) by Fujiwara in 1980, several animal-derived natural surfactants and synthetic surfactants have been developed. Synthetic surfactants were designed to overcome limitations of natural surfactants such as cost, immune reactions, and infections elicited by animal proteins contained in natural surfactants. However, first-generation synthetic surfactants that are protein-free have failed to prove their superiority over natural surfactants because they lack surfactant protein (SP). Lucinactant, a second-generation synthetic surfactant containing the SP-B analog, was better or at least as effective as the natural surfactant, suggesting that lucinactant could act an alternative to natural surfactants. Lucinactant was approved by the U. S. Food and Drug Administration in March 2012 as the fifth surfactant to treat neonatal RDS. CHF5633, a second-generation synthetic surfactant containing SP-B and SP-C analogs, was effective and safe in a human multicenter cohort study for preterm infants. Many comparative studies of natural surfactants used worldwide have reported different efficacies for different preparations. However, these differences are believed to due to site variations, not actual differences. The more important thing than the composition of the surfactant in improving outcome is the timing and mode of administration of the surfactant. Novel synthetic surfactants containing synthetic phospholipid incorporated with SP-B and SP-C analogs will potentially represent alternatives to natural surfactants in the future, while improvement of treatment modalities with less-invasive or noninvasive methods of surfactant administration will be the most important task to be resolved.

Signal Transduction Mechanisms Mediating Surfactant Phospholipid Secretion in Isolated Type II Cell (Type II Cell 분리체로부터 Surfactant 인지질의 분비를 매개하는 신호변환 기전)

  • Park, Sung-Soo
    • Tuberculosis and Respiratory Diseases
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    • v.43 no.2
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    • pp.123-127
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    • 1996
  • Secretion of surfactant phospholipid can be stimulated by a variety of agonists acting via at least three different signal transduction mechanisms. These include the adenylate cyclase system with activation of cAMP-dependent protein kinase; activation of protein kinase C either directly or subsequent to activation of phosphoinositide-specific phospholipase C and generation of diacylglycerols and inositol trisphosphate; and a third mechanism that involves incresed $Ca^{2+}$ levels and a calmodulin-dependent step. ATP stimulates secretion via all three mechanisms. The protein kinase C pathway is also coupled to phopholipase D which, acting on relatively abundant cellular phospholipids, generates diacylglycerols that further activate protein kinase C. Sustained protein kinase C activation can maintain phosphatidylcholine secretion for a prolonged period of time. It is likely that interactions between the different signaling pathways have an important role in the overall physiological regulation of surfactant secretion.

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Changes of [A-a] gas Gradient in Rabbits with Oxygen Toxicity (산소중독시 가토의 [A-a] gas Gradient 의 변화)

  • 이두연
    • Journal of Chest Surgery
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    • v.20 no.1
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    • pp.1-12
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    • 1987
  • Respiratory care with oxygen inhalation is often a necessity to maintain life, and it is one of the important therapeutic adjuncts in respiratory disease and in intensive care after surgery. However, it has been reported that oxygen toxicity occurs after prolonged exposure to 100% 0, [Smith, 1899; Kistler et al. 1967; Schaffner et al. 1967; Rowland and Newman, 1969. Subjective symptoms of oxygen toxicity include tracheal irritation, frequent cough, some burning sensation in the trachea, tachypnea, severe dyspnea, etc. [Welch, 1963; Fisher et al, 1968; Milier et al, 1970; Clark and Lambertsen, 1971; Sackner, 1975]. Pathologic findings are atelectasis, injuries to the pulmonary capillaries and hemorrhage in the alveoli in gross specimens. There can be inflammation, proliferation of fibrin, thickening of alveolar membranes, degeneration of collagen fibers and interstitial edema in the microscopic findings. [Penrod, 1956; Cedergren, 1959; Bean, 1965; Schaffner, 1967]. Dubois and colleagues [1961] found that the amount of pulmonary surfactant was decreased in oxygen toxicity and atelectasis followed by the decreased pulmonary surfactant. Many authors reported that vital capacity, inspiratory force, pulmonary compliance, pulmonary capillary blood flow and pulmonary elasticity were deceased and arteriovenous shunting increased. [Comroe et al, 1945; Fuson et al, 1965; Kistler et al, 1966; Knowles and Blenner-hassett, 1967; Barber et al, 1978]. Many human volunteers were examined after prolonged exposure in a high oxygenated chamber and there were a few reports on animals with oxygen toxicity, subjects including rabbits. Gas partial pressures of alveoli and arteries were measured in rabbits exposed to 100% $O_2$ and the alveolar-arterial gas gradients were analyzed, which is the basis for the study of oxygen toxicity. These rabbits were divided into two groups; rabbits under natural respiration, and second group under artificial respiration with a respirator. The alveolar $PO_2$ [$P]AO_2$] and $PCO_2$ [$PACO_2$], and the arterial $PO_2$ [$PaO_2$] were measured under varying $O_2$ pressures; 15% $O_2$, 21% $O_2$ and 100% $O_2$.

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A Case of Pulmonary Alveolar Proteinosis (폐포단백증 1예)

  • Woo, Dae-Hyung;Park, Jung-Eun;Ryu, Yung-Ha;Kim, Hyun-Jung;Shin, Kyeong-Cheol;Chung, Jin-Hong;Lee, Kwan-Ho
    • Journal of Yeungnam Medical Science
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    • v.27 no.1
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    • pp.57-62
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    • 2010
  • Pulmonary alveolar proteinosis (PAP) is a rare disorder that's characterized by accumulation of surfactant components in the alveolar space. Idiopathic PAP is recognized as an autoimmune disease that's due to impaired alveolar macrophage function and this caused by autoantibodies against granulocyte-macrophage colony-stimulating factor (GM-CSF). We report here a case of pulmonary alveolar proteinosis that was deemed interstitial lung disease at the initial diagnosis. A 61-year-old man presented with intermittent blood tinged sputum and dyspnea on exertion. The man was a painter for 30 years and he had a 10 pack-years smoking history. Chest computerized tomography (CT) revealed multifocal ground-glass opacity with interstitial thickening at both lungs. His pulmonary function tests and methacholine test revealed non specific results. He was diagnosed with interstitial lung disease on the basis of the chest CT finding and occupational history. However, seven months later, his symptoms progressed. Follow-up chest CT was performed. Wedge resection via video-assisted thoracoscopic surgery (the anterior basal segment of the left lower lobe) was done. Microscopic examination showed large groups of alveoli with excessive amounts of surfactant and a complex mixture of protein and lipid (fat) molecules. Finally, he was diagnosed as having pulmonary alveolar proteinosis.

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Analysis of Pulmonary Surfactant after Intratracheal Instillation of SWNCT and MWCNT (SWCNT 및 MWCNT의 기관내 점적주입 후 폐 계면활성제의 분석)

  • Lee, Byeongwoo;Seo, Jungkwan;Shim, Ilseob;Eom, Igchun;Kim, Plije
    • Journal of Environmental Health Sciences
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    • v.43 no.4
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    • pp.273-279
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    • 2017
  • Objectives: Carbon nanotubes (CNTs) are next-generation industrial nanoparticles which possess excellent mechanical strength along with good thermal conductivity and electric properties. Given these characteristics, carbon nanotubes are being widely applied in various fields, including research and development. However, concerns have been raised over hazardous properties due to their similar fiber shape to asbestos. Recent studies have shown that CNTs pose potential hazards which may cause fibrosis and/or lung inflammation similarly to asbestos. Methods: After intratracheal instillation of SWCNTs and MWCNTs to rats, pulmonary surfactant (PS) of the SWCNTs and MWCNTs was measured and analyzed using bronchoalveolar lavage fluid collected from the lung. After a single intratracheal instillation of SWCNTs and MWCNTs, phospholipid predominantly showed a significant increase compared to the control group, while proteins exhibited a significant increase both three days and one week after instillation. Results: As a result of surface tension, MWCNTs showed a significant decrease three days after treatment compared to the control group. In the case of the total cell number three days after instillation, MWCNTs revealed a temporarily significant increase when compared to the control group. For PMN number, when compared to the control group, SWCNTs displayed a significant increase throughout the observation period, while MWCNTs showed a significant increase three days and three months after treatment. Conclusions: After exposure to CNTs, the total cell number and PNT number, which indicate inflammatory response, were significantly increased. Therefore, this study suggests fiber-shaped CNTs may have a harmful effect on the lungs.

Experimental Study of Surface Activity in Acute Pulmonary Edema (급성 폐수종에서의 Pulmonary Surfactant 에 관한 연구)

  • 김진식;홍완일
    • Journal of Chest Surgery
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    • v.7 no.1
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    • pp.1-8
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    • 1974
  • Acute pulmonary edema was induced by intravenous injection of epinephrine, intravenous infusion of dextran and intratracheal instillation of acid solution index was determined from pressure volume curves in excised lungs. Surface activity was also investigated with measurements of maximum and minimum surface tension and stability index on saline extracts of same lungs. The results were as follows. 1. The expansion index of excised lung in which pulmonary edema was induced by intravenous injection of epinephrine, intravenous infusion of dextran and intratracheal instillation of acid solution was ignificantly decreased as compared with the normal control of $0.86{\pm}0.017$ to $0.74{\pm}0.03$, $0.71{\pm}0.081$and $0.76{\pm}0.02$, respectively. 2. The deflation curves of excised lungs in which pulmonary edema was induced were significantly decreased as compared with the normal controls. 3. The minimum surface tension of excised lung in which pulmonary edema was induced was significantly increased in each groups and stability index was significantly decreased as compared with the normal controls 0.78 to $0.35{\pm}0.039$, $0.29{\pm}0.02 $ and $0.31{\pm}0.083$, respectively. 4. The decrease of pulmonary surface activity in acute pulmonary edema was in proportion to the degree of pulmonary edema regardless of their etiology.

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