Background

Lung alveolarization, the development of the alveoli, is disturbed in preterm infants with bronchopulmonary dysplasia (BPD), the most common complication of preterm birth. Animal models based on oxygen toxicity to the developing mouse lung are used to understand the mechanisms of stunted alveolarization in BPD, and to develop new medical management strategies for affected infants. The toxicity of genetic and pharmacological interventions, together with maternal cannibalism, reduce mouse litter sizes in experimental studies. The impact of litter size on normal and stunted lung alveolarization is unknown, but may influence data interpretation. The aim of the study was to assess the impact of litter size on normal and oxygen-stunted lung alveolarization in mice.

Methods

BPD was experimentally modelled in newborn C57BL/6J mice by exposure to 85% O₂ in the inspired air for the first 14 days of post-natal life. Perturbations to mouse lung architecture were assessed by design-based stereology, in which the alveolar density, total number of alveoli, gas-exchange surface area, and the septal thickness were estimated.

Results

Litter sizes of a single mouse were not viable to post-natal day 14. Normal lung alveolarization was comparable in mouse pups in litters of 2, 4, 6, and 8 pups per litter. Hyperoxia was equally effective at stunting lung alveolarization in mouse pups in litters of 2, 4, 6, and 8 pups per litter.

Conclusions

Studies on normal lung alveolarization as well as alveolarization stunted by oxygen toxicity can be undertaken in mouse litters as small as two pups, and as large as eight pups. There is no evidence to suggest that data cannot be compared within and between litters of two to eight mouse pups.

中文翻译：

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产仔量对新生小鼠幼崽存活，生长和肺泡化的影响。

背景

在患有早产儿最常见并发症的支气管肺发育不良（BPD）的早产儿，肺泡化，肺泡的发育受到干扰。基于对发育中的小鼠肺部的氧气毒性的动物模型可用于了解BPD中肺泡发育迟缓的机制，并为患病的婴儿制定新的医学管理策略。在实验研究中，遗传和药理学干预的毒性以及母亲的同类相食会减少小鼠垫料的大小。产仔数对正常肺泡发育和发育不良的影响尚不清楚，但可能会影响数据解释。该研究的目的是评估小鼠产仔数对正常和氧致肺肺泡化的影响。

方法

在出生后前14天，通过在吸入的空气中暴露85％的O ₂对新生C57BL / 6J小鼠进行BPD实验建模。通过基于设计的立体学评估对小鼠肺结构的扰动，其中估计了肺泡密度，肺泡总数，气体交换表面积和间隔厚度。

结果

一只小鼠的产仔数在出生后第14天不可行。正常的肺泡化在每窝2，4、6和8窝的小鼠中可比。高氧血症在每窝产仔数为2、4、6、8的幼仔中，在阻止幼仔的肺泡发育方面同样有效。

结论

正常的肺泡化以及因氧气中毒而导致的肺泡化的研究可以在小至两只幼崽和八只幼崽的小鼠垫料中进行。没有证据表明不能在两到八个小鼠幼仔之间和之间进行数据比较。