{'fraction_non_alphanumeric': 0.054906542056074766, 'fraction_numerical': 0.04205607476635514, 'mean_word_length': 4.403785488958991, 'pattern_counts': {'":': 0, '<': 2, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Effect of lethal hyperoxia on pulmonary development and lung injury in neonatal rats].

OBJECTIVE
To study the effect of oxygen at lethal levels (95%) on pulmonary development and lung injury in neonatal rats and establish rat models of bronchopulmonary dysplasia.


METHODS
Three-day-old and adult SD rats were assigned to experimental or control groups and subjected to 95% O(2) exposure and room air for 7 days. Body weight and length of the rats were recorded, and histological study of the lung tissue and radical alveoli count (RAC) were carried out.


RESULTS
The mortality rate of the neonatal and adult rats was 12.5% and 35.2% in hyperoxia group, respectively. The newborn rats in hyperoxic group had lower body weight (18.02-/+0.68 vs 13.24-/+0.59 g) and length (8.83-/+0.25 vs 6.76-/+0.51 cm) than those in the control group (P<0.05), with also lower RAC (9.50-/+1.05 vs 13.00-/+1.79, P<0.05); RAC of the adult rats with hyperoxic exposure (12.67-/+2.25) was higher that of exposed neonatal rats, but not significantly different from that of the adult or neonatal rats in the control group (P>0.05). Structure configuration of the rats on the first 10 days of life resembled that of adulthood. The lung of hyperoxic neonatal rats showed thinner walls of alveoli, simple alveolar structure, fewer and larger alveoli, expanded and shrunk alveoli, while the lung of the adult rats displayed thicker septa, smaller space of alveoli, and cells in the space of the alveoli.


CONCLUSION
Exposure of neonatal rats to 95% O(2) may result in mild pulmonary inflammation in addition to growth impediment and impaired lung development, which shares morphologic similarities to human bronchopulmonary dysplasia.