Abstract
The etiology and pathogenesis of neonatal and adult respiratory distress syndromes (RDS) differ widely but share the characteristic inability of the lungs to adequately oxygenate the blood. Neonatal RDS occurs in premature infants deficient in surfactant (SRF) [1]. SRF deficiency causes alveoli to collapse on expiration, resulting in progressive respiratory failure. Because neonatal RDS directly reflects deficiency of surfactant, various investigators have tried therapeutic administration of heterologous, artificial, and homologous surfactants [2–4]. These preparations generally lower surface tension in vitro and in animal models, and are reported to be efficacious in infants with RDS.
Supported in part by USPHS grants HD 10622 and HD 16292 (T. A. Merritt), FDA grant FDA-R-000112 (T. A. Merritt and D. S. Strayer), HL 23584 (R. Spragg), a grant from the March of Dimes (T. A. Merritt), and a grant from the Finnish Academy of Sciences (M. Hallman).
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Keywords
- Immune Complex
- Adult Respiratory Distress Syndrome
- Pulmonary Surfactant
- Congenital Toxoplasmosis
- Neonatal Respiratory Distress Syndrome
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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© 1988 Springer-Verlag Berlin Heidelberg
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Strayer, D.S., Merritt, T.A., Spragg, R., Hallman, M. (1988). Immunogenicity of Surfactant and Its Implications for Replacement Therapy. In: Lachmann, B. (eds) Surfactant Replacement Therapy. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73305-5_35
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DOI: https://doi.org/10.1007/978-3-642-73305-5_35
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