Surface Tension:  Surface tension is measured experimentally as a force acting across an imaginary line 1 cm long on the surface of a liquid (the force of which is measured in dynes).  When you were a young child, one of your parents probably showed you how a sewing needle could be placed very carefully on top of a dish of water, and the needle would float.  This was because molecules of water are attracted to one another; the water molecules holding on to one another under the pin hold the pin afloat!  We known that a drop of water on a table top will not spread out into a layer which is one molecule thin; again, water molecules are attracted to one another, and they pile up (surface tension) rather than spreading out into such a thin layer!

Above is a very clever photograph of a soap bubble (the media is, of course, water) by Walter Wick, whose book "A Drop of Water" is a must read if you have little children interested in science and water!  (Scholastic Press, 1997. ISBN 0-590-22197-3).  Detergents reduce surface tension in fluids... this means that the bubble (which is ostensibly a sphere of water filled with air) is less likely to collapse than if it did not contain soap!

In a bubble, surface tension, or the attraction between water molecules, is trying to collapse the bubble.  The inward force in a small bubble is greater than the inward force in a larger bubble containing the same amount of water.  That means that the inward force in a small bubble is sufficient to make a larger bubble expand and burst!  This strange sounding relationship means that there is more "collapsing force" exerted within a small bubble than in a larger bubble containing the same amount of water.  Perhaps an even simpler way to understand this mathematical concept is to examine LaPlace's Law.

Figure: Direction of Forces Trying to Collapse a Bubble

All of the water molecules in the walls of the bubble are trying to move closer to one another.  The net effect is to reduce the surface area of the bubble, at the same time reducing the diameter of the bubble and collapsing the overall size of the bubble!

Now, think of the alveoli in the lung as bubbles.  Alveoli are spherical, like bubbles, and the alveoli are lined with fluid.  Constant fluid secretion keeps the alveolar lining moist!  Remember, the alveolar tissue is living tissue and if it is not bathed in fluid it will die.  The skin cells covering our body are not bathed in fluid, but that is because our outermost epidermal layers are not living tissue!

As we inhale, our lungs expand and the surface area of the "bubbles" (alveoli) increase.  This means that, as we inhale, there is a decrease in the inward pressure associated with surface tension trying to collapse our lungs.  Note however, that as we inflate our lungs, we stretch elastic tissues within our lungs and chest wall that will make our lungs collapse back down as we exhale!

As we exhale, our lungs are reduced in size and the surface area of the bubbles (alveoli) decrease.  This means that, as we exhale, there is an increase in the inward pressure associated with surface tension trying to collapse our lungs.  Note however, that as we deflate our lungs, the elastic tissues are brought closer to resting position, and so the elastic tissues do not work as hard to collapse our lungs!

The lung has a special way to decrease surface tension in the alveolar walls.  In the alveolar walls are "surfactant cells" (type II pneumocytes).  Surfactant cells are large cells with big, plump nuclei that easily differentiate them from alveolar and capillary endothelial cells.  Surfactant cells secrete surfactant, a mixture of protein-phospholipid complexes which acts like a strong detergent (Surfactant Protein B and C: SP-B & SP-C).  Recall that detergents reduce surface tension, reducing the pressure trying to collapse bubbles!  The primary constituent of surfactant is a phospholipid called dipalmitoyl lecithin or dipalmitoyl phosphatidyl choline (ie. a phosphatidyl choline - fatty acid complex).  Evidence of the presence of surfactant can be seen in fluid collected from the airways of victims of pulmonary edema; this fluid contains bubbles which are very stable and remain for hours after the time of death.

Oh, by the way, good sources of lecithin are soybean, corn and egg yolks!

The surface tension of water is high and constant, regardless of surface area.  However, when we add pulmonary surfactant, the surface tension of water is reduced.  Pulmonary surfactant would make a strong detergent because it strongly decreases surface tension!  As the area of the bubble (alveolus) is decreased, pulmonary surfactant prevents the inward pressure associated with surface tension of fluid in the alveoli from rising too high.  This decrease in surface tension structurally stabilizes the alveolar sacs, thereby decreasing the overall pressure trying to collapse the alveoli.  Thus, the presence of surfactant prevents the alveoli from collapsing under the normal surface tension exerted by the aqueous fluid lining the alveolar surfaces.  The bottom line is that surfactant is necessary to prevent your lungs from collapsing!

Role of Surfactant (Dipalmitoyl phosphatidyl choline):

1) To decrease the surface tension of fluid lining the alveoli, reducing the likelihood that the lung will collapse!

2) To increase the compliance of the normal lung so that less work is expended for breathing!

3) Surfactant helps keep the alveoli relatively "dry" - a high surface tension would suck fluid away from the alveolar walls into the alveolar space but with the decreased surface tension provided by surfactant, the alveolar space is maintained in a "relatively dry state" (ie. the alveoli are covered with a thin fluid layer rather than filling up with fluid).

How does surfactant do this?  Simple!  Surfactant is a phospholipid.  The phosphate head groups of the surfactant molecules are hydrophilic... that is, they are attracted to water molecules.  As surfactant molecules pull on water molecules, they pull the water molecules apart from other water molecules, causing the attractive forces pulling the water molecules together to be reduced.

Hyaline Membrane Disease (HMD = Insufficient Surfactant) in the Newborn; also known as Respiratory Distress Syndrome (RDS):

A lack of surfactant may lead to death.  Premature infants may not have synthesized sufficient surfactant to line the alveoli.  Although an insufficiency of surfactant can be seen in any newborn infant, most are producing sufficient surfactant by 26-28 weeks of gestation.  That means, if you hear about a premature infant born prior to 26-28 weeks gestation, among all the other problems you should be thinking about... be sure to include very labored breathing, because they will not have sufficient surfactant.  Alveolar collapse may occur.  The infant appears to be working very hard to ventilate the lungs because he or she is.  They often become very pale and cold because of poor gas exchange!  Surfactant molecules and O₂ can be administered with a vaporizer (atomizer, aerosolizer) in an incubator for several days, until such time as the lungs are sufficiently developed to take over this function on their own.  Some of these infants may require ventilator assisted oxygenation, which leads to production of oxygen-derived free radicals.  Free radicals may, in turn, lead to bronchpulmonary dysplasia (BPS) (epithelial hyperplasia), which may lead to several months of respiratory distress syndrome (RDS).  Infants receiving ventilatory assistance and developing RDS are at risk for patent ductus arteriosus.  Some of these premature infants may have additional pathologies. The term hyaline membrane refers to degenerating membranes; here, to the fibrous, necrotic appearance of the alveolar epithelium along with its pink-staining protein exudate that may develop within hours of birth in surfactant insufficient newborns.

Now the story gets even worse... the gene for production of SP-B (surfactant protein-B) may be defective, in which case the infant has no chance of ever producing normal surfactant.  There appear to be several variants of the genetic mutation and neither the frequency nor genotype-phenotype correlations have been worked out!  These infants are invariably lost if a lung transplant is not available!

Acute Lung Injury (ALI) and Respiratory Distress Syndrome (RDS):  Acute lung injuries might include gas poisonings, inhalation of toxic or caustic substances, extreme smoke inhalation, pneumonia, other bacterial or viral infections or other causes of sepsis.  In any of these circumstances, it is possible that sufficient Type II pneumocytes might be damaged to reduce surfactant production to critically low levels.  Thus, the term ALI is associated with surfactant insufficiency resulting from trauma to the lung.  The prognosis is poor and survival rate is around 50%.  Either the lungs must be given time to heal or a lung transplant must occur.