肺表面活性物质相关蛋白的特性研究

肺表面活性物质相关蛋白的特性研究谢尔凡（第三军医大学烧伤研究所,重庆６３００３８）关键词肺表面活性物质,表面活性物质相关蛋白肺表面活性物质是由脂质和蛋白质组成的复合物,其主要生理功能是降低肺泡表面张力,维持肺泡结构相对稳定。近年来,特异性的肺表面活性...     

肺表面活性物质的临床应用研究进展

国内外研究表明,肺表面活性物质(pulmonary surfactant,PS)异常与急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)的发生、发展关系密切。因此,临床上对外源性肺表面活性物质制剂的替代疗法也日益重视。本文就肺表面活性物质的功能、急性肺损伤后的变化及其治疗急性肺损伤的相关研究作一综述。     

肺的分泌功能

很长时间,肺一直被认为是单纯的呼吸器官。近年来,人们越来越认识到,肺不仅是呼吸器官,而且参与了许多生物活性物质的合成、激活、释放、分解和转化功能。下面分别讨论肺与各类生物活性物质的关系。１肺泡表面活性物质肺泡表面活性物（ＰｕｌｍｏｎａｒｙＳｕｒｆａｃ...     

肺表面活性蛋白C基因异常与婴幼儿肺间质性疾病

肺表面活性蛋白C（surfactant protein C,SP-C）基因是目前被发现的唯一仅在肺泡Ⅱ型上皮细胞中表达的肺表面活性蛋白基因,其蛋白表达产物SP-C是构成肺表面活性物质的小分子疏水性蛋白之一,具有调节肺泡液.气界表面张力、维持肺表面活性膜的稳定及参与肺器官局部防御体系等重要的生理功能.SP-C基因异常可造成SP-C结构变化和功能丧失,从而导致各种婴幼儿肺疾病,其中,肺间质性疾病（interstitial lung disease,ILD）的发病与SP-C基因突变的关系尤为密切.     

肺表面活性物质的防御保护功能

肺表面活性物质（ＰＳ）除能降低表面张力外,还具有抗氧化、抗感染、促进肺内异物颗粒的排出,减轻变态反应性及弹性蛋白酶所致的肺损伤等多方面的防御保护功能。ＰＳ是肺内特有的生理性抗损伤因子。     

肺表面活性物质相关蛋白D研究进展

肺表面活性物质相关蛋白Ｄ研究进展谢尔凡（第三军医大学西南医院烧伤研究所,重庆６３００３８）关键词肺表面活性物质相关蛋白Ｄ肺表面活性物质（ＰＳ）由脂质和蛋白质组成,其主要生理功能包括降低肺泡表面张力,维持肺泡结构相对稳定,防止肺萎陷和肺水肿,参与宿主呼...     

疏水性肺表面活性物质蛋白的结构研究进展

疏水性肺表面活性物质蛋白（ＳＰ）包括ＳＰ－Ｂ和ＳＰ－Ｃ,它们在决定肺表面活性物质的结构、代谢及功能等方面有重要作用。ＳＰ－Ｂ和ＳＰ－Ｃ功能的多样性可能与其结构的特殊性有关,在表达及合成的过程中,二的结构均经过了复杂的加工,使之能与脂质系统相互作用以发挥其生理功能。     

肺表面活性物质的研究

肺表面活性物质的研究□刘桂萍（吉林省白城师范高等专科学校生物系，白城１３７０００）□付晶（吉林省长春市宽城区中医院，长春１３００５１）肺表面活性物质（ｐｕｌｍｏｎａｒｙｓｕｒｆａｃｔａｎｔ，ＰＳ）这一概念首先是由德国生理学家ＶｏｎＮｅｅ－ｇａａｒｄ在...     

山莨菪碱对家兔油酸型肺水肿肺表面活性物质含量的影响

急性肺水肿是多种原因引起的呼吸窘迫综合征(RDs)的早期基本病理变化〔’〕,其中,肺表面活性物质的质和量的异常会影响这一病理生理过程〔2〕。但目前对肺表面活性物质在此病理过程中的变化认识并不深人,许多问题还处在探讨阶段。为了探求RDS时急性肺水肿的机制及寻找有效的防治药物,本研究276Chin J ApPI Physiol 1992;8(3)采用静脉注射油酸引起急性肺水肿作为模型,观察肺表面活性物质含量的变化及山食若碱(654一2)对其含量的影响,以进一步探讨654一2与肺表面活性物质的关系及654一2抗肺水肿的防治机理。1材料和方法l.l动物分组及处理…     

大鼠冷暴露后肺表面活性物质的变化

大鼠冷暴露后肺表面活性物质的变化张秀琳王月燕刘改香刘明远（济南军区医学高等专科学校生理教研室,济南２５００２２）肺表面活性物质（ＰＳ）除具有降低肺泡表面张力的作用外,还在下呼吸道防御机制中起重要作用。急性冷暴露后易患呼吸系统感染及加重诱发某些呼吸系统...     

Surfactant and its role in the pathobiology of pulmonary infection

Pulmonary surfactant is a complex surface-active substance comprised of key phospholipids and proteins that has many essential functions. Surfactant's unique composition is integrally related to its surface-active properties, its critical role in host defense, and emerging immunomodulatory activities ascribed to surfactant lipids. Together these effector functions provide for lung stability and protection from a barrage of potentially virulent infectious pathogens.     

Surfactant alteration and replacement in acute respiratory distress syndrome

The acute respiratory distress syndrome (ARDS) is a frequent, life-threatening disease in which a marked increase in alveolar surface tension has been repeatedly observed. It is caused by factors including a lack of surface-active compounds, changes in the phospholipid, fatty acid, neutral lipid, and surfactant apoprotein composition, imbalance of the extracellular surfactant subtype distribution, inhibition of surfactant function by plasma protein leakage, incorporation of surfactant phospholipids and apoproteins into polymerizing fibrin, and damage/inhibition of surfactant compounds by inflammatory mediators. There is now good evidence that these surfactant abnormalities promote alveolar instability and collapse and, consequently, loss of compliance and the profound gas exchange abnormalities seen in ARDS. An acute improvement of gas exchange properties together with a far-reaching restoration of surfactant properties was encountered in recently performed pilot studies. Here we summarize what is known about the kind and severity of surfactant changes occuring in ARDS, the contribution of these changes to lung failure, and the role of surfactant administration for therapy of ARDS.     

Surfactant proteins A and D in the genital tract of mares

The presence of surface-active material in the lung alveolus has been known for several decades as being essential for normal lung function. Surfactant is essential for reducing the surface tension at the alveolar air-liquid interface. Pulmonary surfactant is composed of 90% lipids and 10% proteins. There are four non-serum proteins surfactant protein-A (SP-A), surfactant protein-B (SP-B), surfactant protein-C (SP-C) and surfactant protein-D (SP-D) named in chronologic order of discovery. Lung SP-A and SP-D belong to a family of collagen-containing C-type lectin family called collectins. The host defence and controlling inflammatory processes of the lung are the major functions of SP-A and SP-D. SP-A and SP-D were originally demonstrated in alveolar type II cells, but recent studies have shown extrapulmonary expression of SP-A and SP-D indicating systemic roles of these proteins. Present study describes the presence of SP-A and SP-D in the mare genital tract, vulva, vagina, ovarium, uterus and tuba uterina using immunohistochemistry and Western blotting. The aim of this study was to characterize surfactant proteins in terms of: (i) whether surfactant proteins were present in the various structures of the mare genital system, (ii) if so, identifying and locating the surfactant proteins and finally (iii) determining the differences from those previously characterized for the lung. Although beyond the scope of this report, it is recognized that there are also some potential implications for better defining the reproductive defence mechanisms in mare. Therefore, genital system organs and tissues from mares were examined. We were able to show that proteins reactive with surfactant-specific antibodies were present in the mare genital tract. Thus, surfactant proteins are present not in just lamellar bodies associated with lung, but also genital system of mare.     

Surfactant phospholipid metabolism

Pulmonary surfactant is essential for life and is composed of a complex lipoprotein-like mixture that lines the inner surface of the lung to prevent alveolar collapse at the end of expiration. The molecular composition of surfactant depends on highly integrated and regulated processes involving its biosynthesis, remodeling, degradation, and intracellular trafficking. Despite its multicomponent composition, the study of surfactant phospholipid metabolism has focused on two predominant components, disaturated phosphatidylcholine that confers surface-tension lowering activities, and phosphatidylglycerol, recently implicated in innate immune defense. Future studies providing a better understanding of the molecular control and physiological relevance of minor surfactant lipid components are needed. This article is part of a Special Issue entitled Phospholipids and Phospholipid Metabolism.     

Surfactant protein A and D in the reproductive tract of stallion

The presence of surface-active material in the lung alveolus has been known for several decades as being essential for normal lung function. The host defense and controlling inflammatory processes of the lung are the major functions of SP-A and SP-D. SP-A and SP-D were originally demonstrated in alveolar type II cells, but recent studies have shown extrapulmonary expression of SP-A and SP-D indicating systemic roles of these proteins. Present study describes the presence of SP-A and SP-D in the stallion genital tract, prepuce, prostate, testis, and seminal vesicle using Western blotting and immunohistochemistry. This paper presents the first evidence for the existence of SP-A and SP-D glycoproteins in the stallion genital tract. We examined genital system organs and tissues from stallion and were able to show that surfactant protein A and D reactive with surfactant-specific antibodies were present in the stallion genital tract tissues and organs. On the basis of results, it can be postulated that surfactant proteins in the stallion reproductive tract contribute to the immune surveillance and to active barrier defense mechanism.     

Surfactant gene polymorphisms and interstitial lung diseases

Pulmonary surfactant is a complex mixture of phospholipids and proteins, which is present in the alveolar lining fluid and is essential for normal lung function. Alterations in surfactant composition have been reported in several interstitial lung diseases (ILDs). Furthermore, a mutation in the surfactant protein C gene that results in complete absence of the protein has been shown to be associated with familial ILD. The role of surfactant in lung disease is therefore drawing increasing attention following the elucidation of the genetic basis underlying its surface expression and the proof of surfactant abnormalities in ILD.     

Eustachian tube surfactant is different from alveolar surfactant: determination of phospholipid composition of porcine eustachian tube lavage fluid.

Phosphatidylcholine (PC) is the main phospholipid in lung surfactant and, more specifically, dipalmitoyl PC (PC16:0/16:0) is the major surface-active component. Several studies have tentatively shown that eustachian tube lavage fluid (ETLF) contains surface-active material. The aim of the present study was to determine, using electrospray ionization mass spectrometry, whether the phospholipid molecular species composition of ETLF is similar to that of lung surfactant. PC was the main component of both ETLF and bronchoalveolar lavage fluid (BALF). The concentration of phosphatidylethanolamine was higher and phosphatidylglycerol was undetectable in ETLF compared with BALF. The molecular species composition of PC in ETLF was notably different from that of BALF, palmitoyloleoyl PC being the major component. Importantly, given its predominance in BALF PC, the concentration of PC16:0/16:0 was low in ETLF. As expected on the basis of this molecular species composition of PC, ETLF did not generate low surface tension values under dynamic compression in a pulsating bubble surfactometer.We conclude that the surfactant in ET is different from lung surfactant, and that low surface tension is not a major determinant of ETLF function.     

Intra- and extracellular compartmentalization of the surface-active fraction in dog lung

Adult mongrel dogs were killed at various times after injection of (3)H-labeled palmitate. The lungs were removed and subjected to an extensive saline lavage. The surface-active fraction was isolated from the lavage and from homogenized residual lung by a procedure based upon differential centrifugation in sucrose solutions. The material isolated from the lavage was designated extracellular surfactant; material from the residual lung was designated intracellular surfactant. Both had similar chemical composition and surface activity. The results of the isotopic labeling studies demonstrate that the two fractions have distinctly different specific activity curves. Label was incorporated into the intracellular surfactant rapidly and reached a peak at 1 hr. No radioactivity was found in the extracellular surfactant for the first 15 min, and the specific activity increased much more slowly than in the intracellular surfactant. These results demonstrate at least two anatomically distinct metabolic "pools" of pulmonary surfactant in the lung. While our data are not conclusive, one possible interpretation is that the biosynthesis of pulmonary surfactant takes place intracellularly with a subsequent secretion onto the alveolar surface.     

Isolation and Characterization of Proteins Associated with the Lung Surfactant System

Rabbit lung washings and purified lung surfactant were delipidated without precipitation or loss of protein. This enabled effective study of the proteins by electrophoretic and immunoelectrophoretlc techniques. The lung washings contained secretory immunoglobulin A and several serum proteins. The protein composition of purified lung surfactant was the same as the unfractionated lung washings confirming our previous study which indicated that there is no specific protein associated with surfactant phospholipids obtained by alveolar lavage with isotonic saline.     

Exposure to Polymers Reverses Inhibition of Pulmonary Surfactant by Serum,Meconium, or Cholesterol in the Captive Bubble Surfactometer

Dysfunction of pulmonary surfactant in the lungs is associated with respiratory pathologies such as acute respiratory distress syndrome or meconium aspiration syndrome. Serum, cholesterol, and meconium have been described as inhibitory agents of surfactant’s interfacial activity once these substances appear in alveolar spaces during lung injury and inflammation. The deleterious action of these agents has been only partly evaluated under physiologically relevant conditions. We have optimized a protocol to assess surfactant inhibition by serum, cholesterol, or meconium in the captive bubble surfactometer. Specific measures of surface activity before and after native surfactant was exposed to inhibitors included i), film formation, ii), readsorption of material from surface-associated reservoirs, and iii), interfacial film dynamics during compression-expansion cycling. Results show that serum creates a steric barrier that impedes surfactant reaching the interface. A mechanical perturbation of this barrier allows native surfactant to compete efficiently with serum to form a highly surface-active film. Exposure of native surfactant to cholesterol or meconium, on the other hand, modifies the compressibility of surfactant films though optimal compressibility properties recover on repetitive compression-expansion cycling. Addition of polymers like dextran or hyaluronic acid to surfactant fully reverses inhibition by serum. These polymers also prevent surfactant inhibition by cholesterol or meconium, suggesting that the protective action of polymers goes beyond the mere enhancement of interfacial adsorption as described by depletion force theories.