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Journal ArticleDOI

Lung phospholipids of human fetuses and infants with and without hyaline membrane disease

TL;DR: The lung phospholipid content and composition were determined on 20 nonbreathing human fetuses and abortuses ranging in gestational age from 2 to 9 months and are compatible with the hypothesis that hyaline membrane disease is due to a prenatal deficiency of lung surfactant.
About: This article is published in The Journal of Pediatrics.The article was published on 1970-11-01. It has received 83 citations till now. The article focuses on the topics: Hyaline & Phospholipid.
Citations
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Journal ArticleDOI
Alan H. Jobe1
TL;DR: In 1959, not long after surfactant had been identified as critical to maintaining lung inflation at low transpulmonary pressures, saline extracts from the lungs of preterm infants with respiratory distress syndrome lacked the low surface tension characteristic of pulmonary Surfactant.
Abstract: In 1959, not long after surfactant had been identified as critical to maintaining lung inflation at low transpulmonary pressures,1,2 Avery and Mead3 reported that saline extracts from the lungs of preterm infants with respiratory distress syndrome lacked the low surface tension characteristic of pulmonary surfactant. After several unsuccessful attempts to treat infants with respiratory distress syndrome with aerosolized surfactant,4,5 intratracheal administration of surfactant recovered from the air spaces of mature animal lungs was found to improve lung expansion and ventilation in preterm animals6–8. The clinical potential of surfactant treatment for respiratory distress syndrome was demonstrated by . . .

611 citations

Journal ArticleDOI
TL;DR: For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfACTant abnormalities may have.
Abstract: Pulmonary surfactant is a complex and highly surface active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume, and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms (immunological, non-biophysical functions). Pulmonary surfactant can only be harvested by lavage procedures, which may disrupt its pre-existing biophysical and biochemical micro-organization. These limitations must always be considered when interpreting ex vivo studies of pulmonary surfactant. A pathophysiological role for surfactant was first appreciated in premature infants with respiratory distress syndrome and hyaline membrane disease, a condition which is nowadays routinely treated with exogenous surfactant replacement. Biochemical surfactant abnormalities of varying degrees have been described in obstructive lung diseases (asthma, bronchiolitis, chronic obstructive pulmonary disease, and following lung transplantation), infectious and suppurative lung diseases (cystic fibrosis, pneumonia, and human immunodeficiency virus), adult respiratory distress syndrome, pulmonary oedema, other diseases specific to infants (chronic lung disease of prematurity, and surfactant protein-B deficiency), interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis), pulmonary alveolar proteinosis, following cardiopulmonary bypass, and in smokers. For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfactant abnormalities may have.

482 citations

Journal Article
TL;DR: Morphometry showed that intraalveolar fibrosis developed in the early proliferative stage and was more prominent than interstitial fibrosis and was the essential factor in the remodels of pulmonary structural remodeling in fibrotic lungs.
Abstract: For a study of the processes and mechanisms of pulmonary structural remodeling in fibrotic lungs and metaplastic squamous epithelial cells in fibrotic alveoli, immunohistochemical, ultrastructural, and light-microscopic morphometric observations were made of the lungs in acute and proliferative stages of diffuse alveolar damage (n = 40) obtained from biopsies and autopsies. Morphometry showed that intraalveolar fibrosis developed in the early proliferative stage and was more prominent than interstitial fibrosis. In the early proliferative stage, activated myofibroblasts migrated into intraalveolar spaces through gaps in the epithelial basement membrane. They then attached to the luminal side of epithelial basement membrane and produced intraalveolar fibrosis and coalescence of alveolar walls. This intraalveolar fibrosis was the essential factor in the remodeled lungs. Albumin, fibrinogen, immunoglobulins, and surfactant apoprotein were present throughout the hyaline membrane. Fibronectin was not found in hyaline membrane of the lesions in early acute stage but was demonstrated in later stages in outer layers of hyaline membranes and in the areas of intraalveolar fibrosis. Fibronectin may be responsible for the migration and proliferation of myofibroblasts in intraalveolar spaces. Metaplastic single-layered and stratified squamous epithelial cells were keratin-positive and surfactant apoprotein-negative. These metaplastic epithelial cells were frequently found in the alveoli with minimal Type II epithelial cell proliferation and in the grossly scarred alveoli.

289 citations

Journal Article
TL;DR: For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfACTant abnormalities may have.
Abstract: Pulmonary surfactant is a complex and highly surface active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume, and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms (immunological, non-biophysical functions). Pulmonary surfactant can only be harvested by lavage procedures, which may disrupt its pre-existing biophysical and biochemical micro-organization. These limitations must always be considered when interpreting ex vivo studies of pulmonary surfactant. A pathophysiological role for surfactant was first appreciated in premature infants with respiratory distress syndrome and hyaline membrane disease, a condition which is nowadays routinely treated with exogenous surfactant replacement. Biochemical surfactant abnormalities of varying degrees have been described in obstructive lung diseases (asthma, bronchiolitis, chronic obstructive pulmonary disease, and following lung transplantation), infectious and suppurative lung diseases (cystic fibrosis, pneumonia, and human immunodeficiency virus), adult respiratory distress syndrome, pulmonary oedema, other diseases specific to infants (chronic lung disease of prematurity, and surfactant protein-B deficiency), interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis), pulmonary alveolar proteinosis, following cardiopulmonary bypass, and in smokers. For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfactant abnormalities may have.

139 citations

Journal ArticleDOI
TL;DR: It is hypothesized that the concentrations of PC16:0/14:0 and PC16-0/16:1 in surfactants correlate with differences in the respiratory physiology of mammalian species, and that their concentrations are adapted to respiratory physiology.
Abstract: Surfactant reduces surface tension at the air-liquid interface of lung alveoli. While dipalmitoylphosphatidylcholine (PC16:0/ 16:0) is its main component, proteins and other phospholipids contribute to the dynamic properties and homeostasis of alveolar surfactant. Among these components are significant amounts of palmitoylmyristoylphosphatidylcholine (PC16:0/ 14:0) and palmitoylpalmitoleoylphosphatidylcholine (PC16:0/ 16:1), whereas in surfactant from the rigid tubular bird lung, PC16:0/14:0 is absent and PC16:0/16:1 strongly diminished. We therefore hypothesized that the concentrations of PC16:0/14:0 and PC16:0/16:1 in surfactants correlate with differences in the respiratory physiology of mammalian species. In surfactants from newborn and adult mice, rats, and pigs, molar fractions of PC16:0/14:0 and PC16:0/16:1 correlated with respiratory rate. Labeling experiments with [methyl-(3)H]choline in mice and perfused rat lungs demonstrated identical alveolar proportions of total and newly synthesized PC16:0/14:0, PC16:0/16:1, and PC16:0/16:0, which were much higher than those of other phosphatidylcholine species. In surfactant from human term and preterm neonates, fractional concentrations not only of PC16:0/16:0 but also of PC16:0/14:0 and PC16:0/ 16:1 increased with maturation. Our data emphasize that PC16:0/14:0 and PC16:0/16:1 may be important surfactant components in alveolar lungs, and that their concentrations are adapted to respiratory physiology.

123 citations


Cites background from "Lung phospholipids of human fetuses..."

  • ...It is essential for normal lung function because it reduces surface tension at the air–liquid interface of alveolar spaces (1, 2, 3)....

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References
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Journal ArticleDOI
TL;DR: Evidence is presented that the material responsible for such a low surface tension is absent in the lungs of infants under 1,100-1,200 gm.
Abstract: Recent observations suggest that a low surface tension may be an important attribute of the lining of the air passages of the lung.1-4The purpose of this paper is to present evidence that the material responsible for such a low surface tension is absent in the lungs of infants under 1,100-1,200 gm. and in those dying with hyaline membrane disease. The role of this deficiency in the pathogenesis of the disease is considered. Surface tension operates so as to minimize the area of the surface. In the lungs, where the internal surface (the alveolar lining) is curved concave to the airway, the tendency of the surface to become smaller promotes collapse. Although the forces not only of surface tension but also of the elastic tissue tend to collapse the lungs, their behavior differs in one important respect. When the lung contains only a small volume of air, the elastic

1,524 citations

Journal ArticleDOI
TL;DR: Human and rat lungs were degassed and filled with air and physiological salt solution for determination of pressure-volume relationships and extracts were prepared from the specimens.
Abstract: Human and rat lungs were degassed and filled with air and physiological salt solution for determination of pressure-volume relationships. Extracts were prepared from the specimens and examined for ...

374 citations

Journal ArticleDOI
TL;DR: An improved procedure for the quantitative assay of phospholipids separated by TLC is described, in which a specially washed Silica Gel H and a newly designed chromatography unit are employed.

365 citations

Journal ArticleDOI
TL;DR: Lung extracts were obtained by either mincing the lungs in saline or by washing the lung with saline through the trachea and no evidence of the presence of sphingomyelin or other surface-active phospholipid was obtained.
Abstract: Lung extracts were obtained by either mincing the lungs in saline or by washing the lung with saline through the trachea. The surface tensions of the extracts on compression to 10% of the original ...

216 citations

Journal ArticleDOI
TL;DR: Although there is good correspondence between the concentrations of lecithin and phosphatidylethanolamine in fetal lung and the enzymatic activities studies in vitro, once breathing begins there is little correspondence between in vivo and in vitro biosynthesis of leCithin by fetuses of the same gestational age.
Abstract: The Biochemical Development of Surface Activity in Mammalian Lung: II. The Biosynthesis of Phospholipids in the Lung of the Developing Rabbit Fetus and Newborn

162 citations