Surface tension characteristically reduces surface area and tends also to reduce volume. The action of this force upon pulmonary alveoli could result in atelectasis if opposing physiological forces were not normally present. There is in man a distending pressure which assists in overcoming the surface forces. However, the distending pressure necessary to maintain inflation of the lungs is extremely low, probably because of a pulmonary surface-active substance, pulmonary surfactant, which is capable of lowering the surface tension almost to zero.1 It is recognized that atelectasis is a predominant pathologic lesion in hyaline-membrane disease. It is, therefore, pertinent to ask these questions: Is there a diminution or absence of surfaceactive substance in this disease? Does pathologic alteration of pulmonary surfactant occur, or is there inactivation of this substance in hyalinemembrane disease? The recent investigation by Adams and associates2 of surface properties and lipids from lungs of infants with hyaline-membrane
HYALINE MEMBRANE DISEASE AND PULMONARY SURFACTANT. JAMA. 1965;192(12):1090. doi:10.1001/jama.1965.03080250068017
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