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1 Pediatric Heart Lung Center, University of Colorado Health Science Center, Denver, Colorado, United States
2 Aurora, Colorado, United States; Pediatric Heart Lung Center, University of Colorado Health Science Center, Denver, Colorado, United States
* To whom correspondence should be addressed. E-mail: anette.kunig{at}uchsc.edu.
VEGF worsens pulmonary edema (PE) during acute lung injury (ALI) while impaired VEGF signaling contributes to decreased lung growth during recovery from ALI due to neonatal hyperoxia. To examine the roles of VEGF in hyperoxia-induced ALI, we hypothesized that rhVEGF treatment during early neonatal hyperoxic lung injury increases PE, but improves late lung structure during recovery. Sprague Dawley rats were placed in 90% oxygen from days 2 to 14. Pups received daily intramuscular injections of rhVEGF165 or saline. On day 14, rats were placed in room air (RA) for 7 days recovery. At days 3, 14, and 21, rats were killed for studies including body weight and wet:dry lung weights; morphometric analysis (radial alveolar counts (RAC), mean linear intercepts (MLI), and vessel density) and lung eNOS protein. Compared to RA, hyperoxia increased PE by histology and wet:dry weights at day 3, which resolved by day 14. Although treatment with rhVEGF did not increase edema in controls, rhVEGF increased wet:dry ratios in hyperoxia rats at days 3 and 14 (p< 0.01). Compared to RA, hyperoxia decreased RAC and increased MLI at days 14 and 21. VEGF treatment increased RAC 181% and decreased MLI 55% on day 14 in the hyperoxia group (p<0.01). On day 21, RAC was increased 176% and MLI was decreased 58% in the hyperoxia group treated with VEGF. rhVEGF treatment during hyperoxia increased eNOS protein on day 3 three-fold (p<0.05). We conclude that rhVEGF treatment during hyperoxia-induced ALI transiently increases PE, but improves lung structure during late recovery.
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