Effect of retinoic acid on lung injury in hyperoxia-exposed newborn rats

Author(s):  
Chang Liwen ◽  
Rong Zhihui ◽  
Zhang Qianshen ◽  
Qian Liling
2000 ◽  
Vol 48 (4) ◽  
pp. 434-444 ◽  
Author(s):  
Kathleen A Veness-Meehan ◽  
Frank G Bottone ◽  
Alan D Stiles
Keyword(s):  

Author(s):  
Chen Hongbing ◽  
Chang Liwen ◽  
Liu Hanchu ◽  
Rong Zhihui ◽  
Zhu Huaping ◽  
...  

1995 ◽  
Vol 4 (6) ◽  
pp. 431-436 ◽  
Author(s):  
M. R. Pierce ◽  
C. A. Voelker ◽  
I. R. S. Sosenko ◽  
S. Bustamante ◽  
S. M. Olister ◽  
...  

We evaluated the effects of sustained perinatal inhibition of NO synthase (NOS) on hyperoxia induced lung injury in newborn rats. NG-nitro-Larginine-methyl-ester (L-NAME) or untreated water was administered to pregnant rats for the final 7 days of gestation and during lactation; followed by postnatal exposure to hyperoxia (>95% O2) or room air. The survival rate of L-NAME treated pups when placed in > 95% O2at birth was significantly lower than controls from day 4 (L-NAME, 87%; control pups, 100%, p < 0.05) to 14 (L-NAME, 0%; control pups, 53%, p < 0.05). Foetal pulmonary artery vasoconstriction was induced by L-NAME with a decrease in internal diameter from 0.88 ± 0.03 mm to 0.64 ± 0.01 mm in controlvs. L-NAME groups (p < 0.05), respectively. We conclude that perinatal NOS inhibition results in pulmonary artery vasoconstriction and a decreased tolerance to hyperoxia induced lung injury in newborn rats.


2018 ◽  
Vol 44 (4-5) ◽  
pp. 226-240 ◽  
Author(s):  
Arben Dedja ◽  
Antonina Gucciardi ◽  
Giuseppe Giordano ◽  
Iole Maria Di Gangi ◽  
Andrea Porzionato ◽  
...  

Author(s):  
Zhang Qianshen ◽  
Chang Liwen ◽  
Liu Hanchu ◽  
Rong Zhihu ◽  
Chen Hongbing

2001 ◽  
Vol 281 (2) ◽  
pp. L336-L344 ◽  
Author(s):  
Richard L. Auten ◽  
S. Nicholas Mason ◽  
David T. Tanaka ◽  
Karen Welty-Wolf ◽  
Mary H. Whorton

Inflammation may contribute to lung injury and impaired alveolar development in bronchopulmonary dysplasia. We treated hyperoxia-exposed newborn rats with antibodies to the neutrophil chemokine cytokine-induced neutrophil chemoattractant-1 (CINC-1) during 95% O2exposure to reduce adverse effects of hyperoxia-induced inflammation on lung development. Rats were exposed at birth to air, 95% O2, or 95% O2+ anti-CINC-1 (injected on days 3 and 4). Bromodeoxyuridine (BrdU) was injected 6 h before death. Anti-CINC-1 treatment improved weight gain but not survival at day 8. Anti-CINC-1 reduced bronchoalveolar lavage neutrophils at day 8 to levels equal to air controls. Total detectable lung CINC-1 was reduced to air control levels. Lung compliance was improved by anti-CINC-1, achieving air control levels in the 10-μg anti-CINC-1 group. Anti-CINC-1 preserved proliferating cell nuclear antigen expression in airway epithelium despite 95% O2exposure. BrdU incorporation was depressed by hyperoxia but preserved by anti-CINC-1 to levels similar to air control. Alveolar volume and surface density were decreased by hyperoxia but preserved by anti-CINC-1 to levels equal to air control. Blockade of neutrophil influx in newborns may avert early lung injury and avoid alveolar developmental arrest that contributes to bronchopulmonary dysplasia.


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