Pulmonary dysfunction in neonatal SP-B-deficient mice
Pulmonary dysfunction in neonatal SP-B-deficient mice
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DOI：
10.1152/ajplung.1997.273.4.l875
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发表时间：
1997-10-01
影响因子：
4.9
通讯作者：
Iwamoto, HS
中科院分区：
文献类型：
--
作者：
Tokieda, K;Whitsett, JA;Iwamoto, HS
对新生的野生型、纯合子和杂合子表面活性蛋白B(SP-B)缺陷小鼠出生后的肺功能进行了评估。SP-B+/+和SP-B+/-小鼠出生后氧合良好，存活。虽然SP-B+/-小鼠的肺顺应性略有下降，但纯合子SP-B-/-小鼠的肺体积和顺应性显著下降。他们在出生后迅速死亡，无法给肺充气或充氧。Western分析显示，SP-B-/-小鼠中SP-B蛋白缺失，SP-B+/-小鼠中SP-B原蛋白减少。SP-B+/-和SP-B-/-小鼠肺表面活性物质蛋白A、表面活性物质原蛋白C、表面活性物质蛋白D和表面活性物质磷脂含量无明显变化。肺饱和磷脂酰胆碱及其前体掺入不受SP-B基因的影响。气管内给予全氟化碳可使SP-B-/-小鼠肺扩张、充氧，延长存活时间，降低SP-B+/+和SP-B+/-小鼠的肺顺应性。SP-B缺乏导致出生时呼吸衰竭，SP-B蛋白减少与肺顺应性降低有关。这些发现证明了SP-B在围产期对空气呼吸的适应中的关键作用。
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.