AJP - Lung Cellular and Molecular Physiology, Vol 273, Issue 4 875-L882, Copyright © 1997 by American Physiological Society

ARTICLES

Pulmonary dysfunction in neonatal SP-B-deficient mice

K. Tokieda, J. A. Whitsett, J. C. Clark, T. E. Weaver, K. Ikeda, K. B. McConnell, A. H. Jobe, M. Ikegami and H. S. Iwamoto
Division of Neonatology, Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039, USA.

Pulmonary function was assessed in newborn wild-type and homozygous and heterozygous surfactant protein B (SP-B)-deficient mice after birth. SP-B +/+ and SP-B+/- mice became well oxygenated and survived postnatally. Although lung compliance was decreased slightly in the SP-B+/- mice, lung volumes and compliances were decreased markedly in homozygous SP-B-/- mice. They died rapidly after birth, failing to inflate their lungs or oxygenate. SP-B proprotein was absent in the SP-B-/- mice and was reduced in the SP-B+/- mice, as assessed by Western analysis. Surfactant protein A, surfactant proprotein C, surfactant protein D, and surfactant phospholipid content in lungs from SP-B+/- and SP-B-/- mice were not altered. Lung saturated phosphatidylcholine and precursor incorporation into saturated phosphatidylcholine were not influenced by SP-B genotype. Intratracheal administration of perfluorocarbon resulted in lung expansion, oxygenation, and prolonged survival of SP-B-/- mice and in reduced lung compliance in SP-B+/+ and SP-B+/- mice. Lack of SP-B caused respiratory failure at birth, and decreased SP-B protein was associated with reduced lung compliance. These findings demonstrate the critical role of SP-B in perinatal adaptation to air breathing.

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