Pulmonary surfactant
From Wikipedia, the free encyclopedia
Pulmonary surfactant is a surface-active lipoprotein formed by type II alveolar cells. The proteins and lipids that comprise surfactant have both a hydrophilic region and a hydrophobic region. By adsorbing to the air-water interface of alveoli with the hydrophilic headgroups in the water and the hydrophobic tails facing towards the air, the main lipid component of surfactant, dipalmitoylphosphatidylcholine, reduces surface tension.
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[edit] Function
- To increase pulmonary compliance
- To prevent the lung from collapsing at the end of expiration
Alveoli can be compared to air bubbles in water, as the alveoli are wet and surround a central air space. The surface tension acts at the air-water interface and tends to make the bubble smaller (by decreasing the surface area of the interface). The gas pressure (P) needed to keep equilibrium between the collapsing force of surface tension (T) and the expanding force of gas in an alveolus of radius r is expressed by the law of LaPlace:
[edit] Compliance
Lung compliance is defined as the volume change per unit of pressure change across the lung. Measurements of lung volume obtained during the controlled inflation/deflation of a normal lung show that the volumes obtained during deflation exceed those during inflation, at a given pressure. This difference in inflation and deflation volumes at a given pressure is called hysteresis and is due to the presence of surfactant. Surfactant causes the surface tension part of elastic recoil observed by von Neergaard. If the lungs did not secrete surfactant, this surface tension would be much higher and it would not be able to inflate normally. The normal surface tension for water is 70 dyn/cm (70 nN/m) and in the lungs it is 25 dyn/cm (25 mN/m); however, at the end of the expiration, compressed surfactant phopholipid molecules decrease the surface tension to very low, near-zero levels. Pulmonary surfactant thus greatly reduces surface tension, increasing compliance allowing the lung to inflate much more easily, thereby eliminating the work of breathing. It reduces the pressure difference needed to allow the lung to inflate. The reduction in surface tension also reduces fluid accumulation in the alveolus as the surface tension draws fluid across the alveolar wall.
Once released into the surface water layer, the surfactant forms a meshwork of tubular myelin. This can be broken down both by macrophages and/or reabsorbed into the lamellar structures of type II cells.
[edit] Alveolar size regulation
As the alveoli increase in size, the surfactant becomes more spread out over the surface of the liquid. This increases surface tension effectively slowing the rate of increase of the alveoli. This also helps all alveoli in the lungs expand at the same rate, as one that increases more quickly will experience a large rise in surface tension slowing its rate of expansion. It also means the rate of shrinking is more regular as if one reduces in size more quickly the surface tension will reduce more so other alveoli can contract more easily than it.
[edit] Composition
[edit] Lipids
d monolayer at the interface. Neutral lipids and cholesterol are also present. The components for these lipids diffuse from the blood into type II alveolar cells where they are assembled and packaged for secretion into secretory organelles called lamellar bodies.
[edit] Proteins
Proteins make up the remaining 10% of surfactant. Half of this 10% is plasma proteins but the rest is formed by the apoproteins SP-A,B,C and D. (SP standing for Surfactant protein.) SP-A and SP-D confer innate immunity as they have carbohydrate recognition domains that allow them to coat bacteria and viruses promoting phagocytosis by macrophages. SP-A is also thought to be involved in a negative feedback mechanism to control the production of surfactant. SP-B and C are hydrophobic membrane proteins that increase the rate that surfactant spreads over the surface. SP-B and SP-C are required for proper biophysical function of the lung.
The apoproteins are produced by the secretory pathway in type II cells. They undergo much post-translational modification, ending up in the lamellar bodies. These are concentric rings of lipid and protein, about 1 µm in diameter. Pulmonary surfactant is secreted by exocytosis.
[edit] Diseases
Infant respiratory distress syndrome (IRDS) is caused by lack of surfactant, commonly suffered by premature babies born before 28-32 weeks of gestation.
Hyaline membrane disease is an older term for IRDS.
