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Effect of postnatal malnutrition on hyperoxia-induced newborn lung development
M M G B Mataloun1, C R Leone, R S Mascaretti
1Pediatria Neonatal, Departamento de Pediatria, Instituto da Criança Prof. Pedro de Alcântara, Universidade de São Paulo, 01230-000 São Paulo, SP, Brasil. mataloun@uol.com.br
Insights
Postnatal malnutrition and hyperoxia worsen lung development in premature rabbits. Combining these factors significantly impairs alveolar growth and lung structure, highlighting the critical role of nutrition in preventing bronchopulmonary dysplasia.
Area of Science:
- Neonatal Physiology
- Pulmonary Medicine
- Nutritional Science
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease affecting premature infants.
- Lung immaturity and hyperoxia are known contributors to BPD.
- The impact of postnatal malnutrition on BPD development remains unclear.
Purpose of the Study:
- To investigate the effects of postnatal malnutrition and hyperoxia on lung development in premature rabbits.
- To assess changes in lung weight, volume, water content, and pulmonary morphometry.
Main Methods:
- Premature rabbits (28-day gestation) were exposed to control or malnourished diets for 7 days.
- Animals were also exposed to room air or hyperoxia (≥95% O2).
- Histological and morphometric analyses were performed on lung tissues.
Main Results:
- Malnutrition decreased lung weight, water content, alveolar number, and fiber content.
- Hyperoxia reduced alveolar number and increased septal thickening.
- The combination of malnutrition and hyperoxia exacerbated alveolar growth arrest and lung remodeling.
Conclusions:
- Postnatal malnutrition intensifies hyperoxia-induced lung injury in premature rabbits.
- Dietary restriction significantly enhances alveolar growth arrest and parenchymal remodeling.
- Adequate postnatal nutrition is crucial for lung development and preventing BPD.
Abstract:
Several factors are associated with bronchopulmonary dysplasia. Among them, hyperoxia and lung immaturity are considered to be fundamental; however, the effect of malnutrition is unknown. Our objective was to evaluate the effects of 7 days of postnatal malnutrition and hyperoxia on lung weight, volume, water content, and pulmonary morphometry of premature rabbits. After c-section, 28-day-old New Zealand white rabbits were randomized into four groups: control diet and room air (CA, N = 17), control diet and > or = 95% O2 (CH, N = 17), malnutrition and room air (MA, N = 18), and malnutrition and > or = 95% O2 (MH, N = 18). Malnutrition was defined as a 30% reduction of all the nutrients provided in the control diet. Treatments were maintained for 7 days, after which histological and morphometric analyses were conducted. Lung slices were stained with hematoxylin-eosin, modified orcein-resorcin or picrosirius. The results of morphometric analysis indicated that postnatal malnutrition decreased lung weight (CA: 0.83 +/- 0.19; CH: 0.96 +/- 0.28; MA: 0.65 +/- 0.17; MH: 0.79 +/- 0.22 g) and water content, as well as the number of alveoli (CA: 12.43 +/- 3.07; CH: 8.85 +/- 1.46; MA: 7.33 +/- 0.88; MH: 6.36 +/- 1.53 x 10-3/mm) and elastic and collagen fibers. Hyperoxia reduced the number of alveoli and increased septal thickening and the mean linear intercept. The reduction of alveolar number, collagen and elastic fibers was intensified when malnutrition and hyperoxia were associated. These data suggest that dietary restriction enhances the magnitude of hyperoxia-induced alveolar growth arrest and lung parenchymal remodeling. It is interesting to consider the important influence of postnatal nutrition upon lung development and bronchopulmonary dysplasia.
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