Protein leaks and surfactant dysfunction in the pathogenesis of respiratory distress syndrome.
This article reviews the phenomenon of surfactant inactivation by soluble proteins. Following surfactant treatment of preterm lambs, the initial clinical response was not maintained. The surface tensions that were low in the lungs following surfactant treatment increased to high values concurrently with the return of severe respiratory failure. The surface properties of the surfactant that remained in the airways and alveoli could be restored if the soluble proteins were removed. These soluble proteins inactivated different surfactants to different degrees and the interaction was very concentration dependent. The proteins entered the lungs of the preterm lamb because of the tendency of these lungs to form pulmonary oedema. Similar surfactant inactivation occurred in the lungs of infants with respiratory distress syndrome. A variety of manipulations influenced the formation of proteinaceous pulmonary oedema, suggesting that new therapeutic strategies could be developed to treat infants with RDS.
Jobe
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Harbor-UCLA Medical Centre, Torrance.
D006801:Humans; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000150:complications; D011654:Pulmonary Edema / Q000150:complications*; D011663:Pulmonary Surfactants / Q000172:deficiency* / Q000502:physiology; D012127:Respiratory Distress Syndrome, Newborn / Q000209:etiology* / Q000503:physiopathology
D011663:Pulmonary Surfactants