Bronchopulmonary dysplasia in a rat model induced by intra-amniotic inflammation and postnatal hyperoxia: morphometric aspects.
Antenatal inflammation is a known risk factor of bronchopulmonary dysplasia. The authors hypothesized that lipopolysaccharide (LPS) administration amplifies hyperoxia-induced lung injury in neonatal rats. LPS (0.5 or 1.0 microg) or normal saline was injected into the amniotic sacs of pregnant rats at 20 d gestation (term 22.5 d). After birth, rats were exposed to 85% oxygen or room air for 1 or 2 wk. Morphometric analysis of lungs was performed on 14 d. One week of hyperoxia without LPS administration resulted in modest lung injury. LPS at 0.5 microg alone did not alter lung morphology, but amplified the effect of 1 wk of hyperoxia resulting in marked inhibition of alveolarization (airspaces were enlarged and alveolar surface areas further reduced). LPS at 1.0 microg independently induced modest lung injury and also amplified the effect of 1 wk of hyperoxia. However, this sensitizing effect of LPS was not observed in rats subjected to 2 wks of hyperoxia, which in itself caused extensive lung injury (possibly masking the effect of LPS). The authors concluded that intra-amniotic LPS sensitizes neonatal rat lungs, and thus, amplifies the hyperoxia-induced inhibition of alveolarization.
Choi
Chang Won
CW
Department of Pediatrics, Seoul National University College of Medicine, Seoul 110-769, Korea.
Kim
Beyong Il
BI
Hong
Joon-Seok
JS
Kim
Ee-Kyung
EK
Kim
Han-Suk
HS
Choi
Jung-Hwan
JH
D000818:Animals; D001997:Bronchopulmonary Dysplasia / Q000209:etiology*; D002821:Chorioamnionitis / Q000139:chemically induced / Q000473:pathology*; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D018496:Hyperoxia / Q000150:complications*; D007231:Infant, Newborn; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000633:toxicity; D008168:Lung / Q000473:pathology*; D011247:Pregnancy; D051381:Rats; D016019:Survival Analysis
D008070:Lipopolysaccharides