Department of Lung Development and Remodelling, Max Planck Institute for Heart and Lung Research, Parkstrasse 1, 60231 Bad Nauheim, Germany; Department of Internal Medicine (Pulmonology), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University, Aulweg 123, 35392 Giessen, Germany.
Department of Internal Medicine (Pulmonology), University of Giessen and Marburg Lung Center (UGMLC), Justus Liebig University, Aulweg 123, 35392 Giessen, Germany; Instituto de Investigación en Biomedicina de Buenos Aires, Godoy Cruz 2390, C1425FQD Ciudad Autónoma de Buenos Aires, Argentina.
Ann Anat. 2020 Nov;232:151579. doi: 10.1016/j.aanat.2020.151579. Epub 2020 Jul 18.
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.
BPD was experimentally modelled in newborn C57BL/6J mice by exposure to 85% O 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.
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.
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.
肺肺泡化是肺泡的发育过程，在患有支气管肺发育不良（BPD）的早产儿中受到干扰，BPD 是早产儿最常见的并发症。基于氧毒性对发育中鼠肺的动物模型用于了解 BPD 中肺泡化发育不良的机制，并为受影响的婴儿开发新的医学管理策略。遗传和药理学干预的毒性以及母鼠的同类相食会降低实验研究中小鼠的产仔数。产仔数对正常和发育不良的肺肺泡化的影响尚不清楚，但可能会影响数据解释。本研究的目的是评估产仔数对正常和氧抑制的鼠肺肺泡化的影响。
通过在出生后 14 天内将 85%的氧气吸入新生 C57BL/6J 小鼠的呼吸空气中，在新生 C57BL/6J 小鼠中实验性地建立 BPD 模型。通过基于设计的体视学评估对小鼠肺结构的干扰，其中估计肺泡密度、肺泡总数、气体交换表面积和间隔厚度。
单只小鼠的产仔数在出生后第 14 天无法存活。在每窝 2、4、6 和 8 只的小鼠幼仔中，正常肺肺泡化是可比的。在每窝 2、4、6 和 8 只的小鼠幼仔中，高氧同样有效地抑制肺肺泡化。
可以在每窝产仔数低至 2 只、高至 8 只的小鼠中进行正常肺肺泡化以及由氧毒性引起的肺泡化发育不良的研究。没有证据表明不能在每窝 2 到 8 只小鼠之间以及每窝内部比较数据。
