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产前饥饿期间胎豚鼠肺表面活性物质含量及Ⅱ型细胞发育

Surfactant content and type II cell development in fetal guinea pig lungs during prenatal starvation.

作者信息

Lin Y, Lechner A J

机构信息

Department of Physiology, St. Louis University School of Medicine, Missouri 63104.

出版信息

Pediatr Res. 1991 Mar;29(3):288-91. doi: 10.1203/00006450-199103000-00013.

DOI:10.1203/00006450-199103000-00013
PMID:2034477
Abstract

Prenatal caloric restriction in guinea pigs causes intrauterine growth retardation and reduced neonatal viability and surfactant phospholipid (PL). We report here fetal surfactant levels in this model, and correlate total lung PL with ultrastructural maturation of surfactant type II cells and lamellar bodies (LB). Pregnant guinea pigs were fed ad libitum throughout their 68-d gestation (control), or fed 50% rations from d 45 until term (starved). Fetal lungs were examined at d 55, 60, and 65 for PL content and composition, including disaturated phosphatidylcholine (DPC), and compared with neonates for both groups. Lung lobes were analyzed ultrastructurally in d 65 fetuses for the numerical, volume, and surface densities of type II cells and the volume densities of LB. Prenatal starvation caused significant intrauterine growth retardation at all ages; body and dry lung weights were reduced on d 65 by 26 and 23%, respectively. By d 55 and thereafter, starvation decreased total lung PL by 43-45% but did not alter PL composition. On d 65, the total lung volumes and relative numbers, surface densities, and volumes of type II cells in tissue and the relative volumes of LB within type II cells did not differ by caloric regimen. Thus, starved and control fetuses had similar total volumes of LB per lung (13-15 microL), although starved animals had significantly less lung DPC. Although the total volume of LB per lung correlated well with total lung DPC from d 55 through birth in controls, starvation led to a significant departure from this relationship.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

豚鼠孕期热量限制会导致子宫内生长迟缓、新生儿存活率降低以及表面活性物质磷脂(PL)减少。我们在此报告该模型中的胎儿表面活性物质水平,并将肺总PL与II型表面活性细胞和板层小体(LB)的超微结构成熟度相关联。怀孕的豚鼠在整个68天的妊娠期自由进食(对照组),或从第45天到足月给予50%的定量食物(饥饿组)。在第55、60和65天检查胎儿肺的PL含量和组成,包括二饱和磷脂酰胆碱(DPC),并将两组与新生儿进行比较。对第65天胎儿的肺叶进行超微结构分析,以确定II型细胞的数量、体积和表面密度以及LB的体积密度。产前饥饿在所有年龄段均导致显著的子宫内生长迟缓;第65天时,体重和肺干重分别降低了26%和23%。到第55天及之后,饥饿使肺总PL减少43 - 45%,但未改变PL组成。在第65天,热量摄入方案对肺总体积、组织中II型细胞的相对数量、表面密度和体积以及II型细胞内LB的相对体积没有影响。因此,饥饿组和对照组胎儿每肺的LB总体积相似(13 - 15微升),尽管饥饿组动物的肺DPC显著减少。虽然在对照组中,从第55天到出生,每肺LB总体积与肺总DPC密切相关,但饥饿导致这种关系出现显著偏差。(摘要截断于250字)

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