CHAPTER 35Pulmonary Function 597animal and distending them alternately with saline and with air
while measuring the intrapulmonary pressure. Because saline
reduces the surface tension to nearly zero, the pressure–volume
curve obtained with saline measures only the tissue elasticity
(Figure 35–12), whereas the curve obtained with air measures
both tissue elasticity and surface tension. The difference be-
tween the two curves, the elasticity due to surface tension, is
much smaller at small than at large lung volumes. The surface
tension is also much lower than the expected surface tension at
a water–air interface of the same dimensions.SURFACTANT
The low surface tension when the alveoli are small is due to the
presence in the fluid lining the alveoli of surfactant, a lipid
surface-tension-lowering agent. Surfactant is a mixture of di-
palmitoylphosphatidylcholine (DPPC), other lipids, and pro-
teins (Table 35–2). If the surface tension is not kept low when
the alveoli become smaller during expiration, they collapse in
accordance with the law of Laplace. In spherical structures like
the alveoli, the distending pressure equals two times the ten-
sion divided by the radius (P = 2T/r); if T is not reduced as r is
reduced, the tension overcomes the distending pressure. Sur-
factant also helps to prevent pulmonary edema. It has been
calculated that if it were not present, the unopposed surface
tension in the alveoli would produce a 20 mm Hg force favor-
ing transudation of fluid from the blood into the alveoli.
Surfactant is produced by type II alveolar epithelial cells
(Figure 35–13). Typical lamellar bodies, membrane-bound
organelles containing whorls of phospholipid, are formed in
these cells and secreted into the alveolar lumen by exocytosis.
Tubes of lipid called tubular myelin form from the extruded
bodies, and the tubular myelin in turn forms the phospholipid
film. Following secretion, the phospholipids of surfactant line
up in the alveoli with their hydrophobic fatty acid tails facing
the alveolar lumen. Surface tension is inversely proportional
to their concentration per unit area. The surfactant molecules
move further apart as the alveoli enlarge during inspiration,
and surface tension increases, whereas it decreases when they
move closer together during expiration. Some of the protein–
lipid complexes in surfactant are taken up by endocytosis in
type II alveolar cells and recycled.
Formation of the phospholipid film is greatly facilitated by
the proteins in surfactant. This material contains four unique
proteins: surfactant protein (SP)-A, SP-B, SP-C, and SP-D. SP-
A is a large glycoprotein and has a collagen-like domain within
its structure. It has multiple functions, including regulation
of the feedback uptake of surfactant by the type II alveolarFIGURE 35–11 Static expiratory pressure–volume curves of
lungs in normal subjects and subjects with severe emphysema
and pulmonary fibrosis. (Modified and reproduced with permission from
Pride NB, Macklem PT: Lung mechanics in disease. In: Handbook of Physiology. Section
3, The Respiratory System. Vol III, part 2. Fishman AP [editor]. American Physiological
Society, 1986.)
FIGURE 35–12 Pressure–volume relations in the lungs of a
cat after removal from the body. Saline: lungs inflated and deflated
with saline to reduce surface tension, resulting in a measurement of
tissue elasticity. Air: lungs inflated (Inf) and deflated (Def) with air re-
sults in a measure of both tissue elasticity and surface tension.
(Reproduced with permission from Morgan TE: Pulmonary surfactant. N Engl J Med
1971;284:1185.)
10 20 30 40012345678Transpulmonary pressure (cm H 2 O)Lung volume (L) FibrosisNormalEmphysema100 Saline Air500
10 20 30 40
Pressure (cm H 2 O)Volume(% maximum inflation)DefInfTABLE 35–2 Approximate composition
of surfactant.Component Percentage Composition
Dipalmitoylphosphatidylcholine 62
Phosphatidylglycerol 5
Other phospholipids 10
Neutral lipids 13
Proteins 8
Carbohydrate 2