Ikegami M, Korfhagen T R, Whitsett J A, Bruno M D, Wert S E, Wada K, Jobe A H
Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039, USA.
Am J Physiol. 1998 Aug;275(2):L247-54. doi: 10.1152/ajplung.1998.275.2.L247.
Mice that are surfactant protein (SP) A deficient [SP-A(-/-)] have no apparent abnormalities in lung function. To understand the contributions of SP-A to surfactant, the biophysical properties and functional characteristics of surfactant from normal [SP-A(+/+)] and SP-A(-/-) mice were evaluated. SP-A-deficient surfactant had a lower buoyant density, a lower percentage of large-aggregate forms, an increased rate of conversion from large-aggregate to small-aggregate forms with surface area cycling, increased sensitivity to inhibition of minimum surface tension by plasma protein, and no tubular myelin by electron microscopy. Nevertheless, large-aggregate surfactants from SP-A(-/-) and SP-A(+/+) mice had similar adsorption rates and improved the lung volume of surfactant-deficient preterm rabbits similarly. Pulmonary edema and death caused by N-nitroso-N-methylurethane-induced lung injury were not different in SP-A(-/-) and SP-A(+/+) mice. The clearance of 125I-labeled SP-A from lungs of SP-A(-/-) mice was slightly slower than from SP-A(+/+) mice. Although the absence of SP-A changed the structure and in vitro properties of surfactant, the in vivo function of surfactant in SP-A(-/-) mice was not changed under the conditions of these experiments.
