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Surfactant is an English made-up word ( surf ace act ive a ge nt ) and means " surface-active substance " (surfactant). The English name has established itself in German for a special, significant surface-active substance in the lungs. Specialized lung cells ( type II pneumocytes ) produce characteristic phospholipids , neutral lipids ( cholesterol esters ) and proteins in a ratio of 10: 1: 1 and some of them are also absorbed from the blood. You will then granules, the lamellar bodies (= osmiophilic granules , stored) and into the alveoli secreted (alveoli), where they make the surface tension decrease (between air and Alveolenauskleidung).

According to the Young-Laplace equation , surface tension is just as important for the small airways (bronchioli), the immature lungs of premature babies that do not yet have alveoli, and the primarily non-alveolar avian lung as it is for the alveolar lungs. This results in an essential significance of a deficiency or inhibition of the surfactant system in acute diseases ( respiratory distress syndrome in premature infants , acute respiratory distress syndrome ).


About 90% of the lipids in the surfactant consist of about 10% neutral lipids (especially cholesterol esters) and 80% phospholipids with a characteristic molecular composition. 80% of them are phosphatidylcholines, which differ in length and degree of saturation of their fatty acids - and thus in their physical properties - from phosphatidylcholines in other organs and secretions (lipoproteins, bile, brain, etc.). Phosphatidylcholines, which are incorporated into the surfactant under the control of the transport protein ABC-A3 , typically have a fatty acid length of 14 or 16 carbon atoms and are saturated ( myristic acid = C14: 0, palmitic acid = C16: 0) or have at most one cis double bond (palmitoleic acid = C16: 1). The three main phosphatidylcholines in the surfactant are therefore dipalmitoyl-phosphatidylcholine (PC16: 0/16: 0), palmitoyl-myristoyl-phosphatidylcholine (PC16: 0/14: 0) and palmitoyl-palmitoleoyl-phosphatidylcholine (PC16: 0/16: 1 ). They basically make up about 75% of the surfactant phosphatidylcholine and are specifically accumulated in the lamellar bodies of type II pneumocytes. Their relative distribution, however, depends on development and respiratory physiology. In particular, PC16: 0/16: 1 is increased in organisms with a high resting respiratory rate, while PC16: 0/14: 0 is increased during alveolar development. A surfactant that essentially contains PC16: 0/16: 0 is only found in birds that have no pulmonary alveoli and stiff lungs in the sense of a flow oxygenator. The classic notion that PC16: 0/16: 0 is the essential main component of the lung surfactant was put into perspective by results that showed that some animals with alveolar lungs have a surfactant almost without this component.

The complex composition of the surfactant in mammals is necessary because of the surface changes in the alveolar gas-liquid boundary during respiration. The alveolar radius and the area become smaller during exhalation, which increases the tendency of the alveoli to collapse at the end of exhalation according to the Young-Laplace equation. In order for the alveoli to remain stable, the surface tension, especially at the end of exhalation , must be close to 0 mN / m (instead of 72 mN / m at an air-water interface). In order to be able to meet the dynamic requirements of the surfactant during the respiratory movements of the alveoli, the surfactant must also contain “fluid” lipids and chaotropic components in addition to the PC16: 0/16: 0, which is rigid at body temperature and packed close to the surface. These are PC16: 0/14: 0, PC16: 0/16: 1 and anionic phospholipids, in particular phosphatidylglycerol and / or phosphatidylinositol, and the hydrophobic surfactant proteins (SP) SP-B and SP-C. In order to maintain the rapid attachment of the surfactant to the interfaces and the breath-synchronous dynamics of the surfactant reservoir and the gas-liquid boundary of the alveoli that oscillate during breathing, these highly hydrophobic proteins SP-B and SP-C are required in addition to the fluid phospholipids interact specifically with the lipids.

In contrast, the hydrophilic surfactant proteins SP-A and SP-D are involved in the regulation of the surfactant development after secretion of the lamellar bodies. Under the action of SP-A together with SP-B, an intermediate stage unpacks the secreted lamellar body into "tubular myelin". This then supplies the surface-associated reservoir. The feedback mechanisms between secretion and reuptake in type II pneumocytes depend on SP-A and SP-D. The latter are also significantly involved in the antibody-independent (primary) defense against bacteria and viruses. In animal experiments z. For example, pneumococcal pneumonia enters the bloodstream in SP-A knockout mice, but not with normal SP-A levels in the lungs.

It is crucial for the surfactant that its composition is adapted to the biology and respiratory physiology of the lungs. If the breathing rate is high, PC16: 0/16: 0 is low and the other fluid components are increased in order to satisfy the dynamic properties of the surfactant. If it is low or if there is no change in the surface of the gas exchange surfaces during the breathing cycle (bird's lungs), PC16: 0/16: 0 is almost the sole surfactant component, together with SP-B to increase the attachment to the interface. The presence of SP-A and SP-D as defense molecules also depends on where inhaled particles settle in the respiratory tract. In humans and mammals these are the alveoli and bronchioles, in birds the air sacs . Accordingly, we find SP-A and SP-D in mammalian surfactant, but not in avian surfactant.


The surfactant lining has at least three interrelated biophysical tasks:

  • Reduction of the "opening pressure" of small alveoli and avoidance of a redistribution of gas from a small alveolus to a large one and thus the collapse of the small one. This shows the dynamic function and structure of the surfactant: The surface tension depends on the density (compression) of the surfactant at the interface, which increases with a smaller radius, which means that the surface tension decreases even further.
  • Increase in lung compliance ( Compliance ), so that a smaller pressure differential and less work of breathing inspiration is needed.
  • Prevents alveolar collapse at the end of exhalation. The intrathoracic pressure on exhalation approaches the alveolar pressure without maneuver and physiologically both around 0 kPa. Under certain circumstances, the intrathoracic pressure can also become slightly positive, for example with forced exhalation with the auxiliary respiratory muscles . According to the Young-Laplace equation, the alveolar radius no longer has to decrease so much in order to balance the equilibrium of collapsing and expanding pressure.

Furthermore, components of the surfactant excreted by the fetus presumably trigger an immune reaction in the maternal uterus, which starts the natural process of initiating the birth of the mature fetus.


Surfactant formation begins from the 24th week of pregnancy, but it is only produced in sufficient quantities from the 34th week of pregnancy (→ lung maturation ), so that premature babies often suffer from respiratory distress syndrome . A diabetic metabolic situation during pregnancy (for example in gestational diabetes ) can also disrupt the development of type II pneumocytes and the formation of surfactant in the fetal period, so that even mature newborns may have too little surfactant. In both cases one speaks of a Newborn Respiratory Distress Syndrome (NRDS). Likewise, in the context of other diseases of the newborn (e.g. in the case of a severe infection or meconium aspiration), there is an increased consumption or the inhibition of surfactants already produced, so that a secondary respiratory distress syndrome can result as a result. A rare but fatal disease is the genetically caused surfactant protein B deficiency, which quickly leads to respiratory distress syndrome in otherwise unremarkable mature newborns. A deficiency in the intracellular transport protein ABC-A3 can have the same consequences. Another disease is the surfactant protein C deficiency, which is accompanied by a chronic surfactant deficiency from birth, but usually only becomes apparent in adulthood in the form of an interstitial lung disease.

Without surfactant, the alveoli fall after birth. the sacculi of immature lungs increasingly collapse, based on the high surface tension and the increased collapse pressure with a small diameter at the end of exhalation (see Young-Laplace equation ). The small airways are also affected by the high surface tension. The gas exchange surface of the lungs is reduced. Gas exchange is hardly or not at all possible and the organism is insufficiently supplied with oxygen and the exhalation of carbon dioxide is impeded. The premature baby suffering from respiratory distress syndrome therefore has cyanosis . The breathing effort increases and manifests itself with "nostrils" and a groaning breath. Ribs and sternum are clearly visible with every breath. If left untreated, a life-threatening clinical picture develops with acute respiratory failure and hypoxia of all other organs.

In the meantime, surfactant extracted or artificially produced from animal lungs can be introduced into the lungs of premature babies as an emulsion via a catheter or tube inserted into the trachea . In addition, if the pregnant woman is expected to give premature birth before 33 weeks of gestational age, two injections of glucocorticoids , usually betamethasone, are given every 24 hours . This increases the amount of surfactant in the child's lungs by accelerating the differentiation of type II pneumocytes , but at the expense of growth, since all glucocorticoids have a catabolic effect. The therapeutic use of surfactant, developed by Tetsuro Fujiwara and others and introduced in the late 1980s, was revolutionary in pediatrics. The chances of survival of small premature babies were significantly improved with this drug.

Damage from long-term exposure to high oxygen partial pressures

Long-term use of very high oxygen partial pressures can also damage the surfactant in adults with the symptoms described above . As the Lorrain-Smith effect, this is particularly relevant for diving, especially for technical diving and hyperbaric oxygen therapy .


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See also

Individual evidence

  1. Jennifer C. Condon, Pancharatnam Jeyasuria, Julie M. Faust, Carole R. Mendelson: Surfactant protein secreted by the maturing mouse fetal lung acts as a hormone that signals the initiation of parturition. In: Proceedings of the National Academy of Sciences . Volume 101, No. 14, 2004, pp. 4978-4983, doi: 10.1073 / pnas.0401124101 .
  2. Erol Tutdibi, Ludwig Gortner: Breathing disorders in the newborn - do genetic factors play a role? University of Saarland. PDF version , accessed May 5, 2013.