Surfactant (dipalmitoylphosphatidylcholine, DPPC) is produced by type II alveolar cells beginning at approximately 24 weeks gestation and reaches functional levels by about 35 weeks. By what physical mechanism does surfactant prevent alveolar collapse (atelectasis) at end-expiration?

• A Surfactant forms a gel that physically bridges opposing alveolar walls to provide structural rigidity and prevent collapse
• B Surfactant reduces alveolar surface tension at low lung volumes by increasing the concentration of DPPC molecules at the air-liquid interface, thereby opposing Laplace's law collapse pressure ✓
• C Surfactant activates alveolar macrophages to produce prostaglandins that relax alveolar smooth muscle during expiration
• D Surfactant reduces alveolar surface tension by binding to and denaturing the surface proteins that normally increase surface tension

Explanation

By the Laplace equation, collapsing pressure = 2T/r (T = surface tension, r = radius). At end-expiration, small alveoli have small radii and would collapse if surface tension were constant. Surfactant (predominantly DPPC) adsorbs at the air-liquid interface and, as alveolar surface area decreases during expiration, DPPC molecules become more concentrated and reduce surface tension from ~70 to <5 mN/m. This near-zero surface tension at small radii markedly reduces the Laplace collapse pressure, maintaining alveolar patency through the respiratory cycle and reducing the work of breathing. Surfactant does not form a structural gel, involve prostaglandins, or denature surface proteins.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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