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Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039
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.
surfactant protein A; transgenic mice; tubular myelin; surface tension; adsorption rate; surfactant treatment
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