INHALED NITRIC OXIDE AFTER OXIDATIVE STRESS IN NEWBORN RATS. EFFECTS ON VEGF EXPRESSION AND ALVEOLARIZATION
Disclosure : This study was supported in part by a grant of the Junta de
Castilla y León (grant No. HUS01A09), Spain.
1 slide(s) – English – 2010-10-23
Background and aims: Exposure of newborn rats to hyperoxia decreases VEGF expression and impairs alveolarization. Much evidence indicates that NO plays a role in VEGF signaling and recent studies have shown that NO induces VEGF synthesis. The purpose of this study was to determine whether inhaled NO improves VEGF expression in the lung tissue and alveolarization after neonatal exposure to oxidative stress.
Methods: Newborn rats were randomized to breathe room air (A), 2 hours A + NO (20 ppm) , 2 hours hypoxia + 2 hours hyperoxia (HH), HH + NO, 2 hours hypoxia + air (HA) or HA + NO. We evaluated pulmonary VEGF in rats at 14 days of life by inmunohistochemistry using 1:100 dilution of rabbit anti-human VEGF (sc-152, Santa Cruz). We used a semiquantitative assessment of VEGF inmunostained, were assigned a relative value from 0 (minimal staining) to 4 (most intense inmunostaining). Quantitative morphometric assessment was done on coded slides with 400x magnification and a eye piece with a sample square grid pattern (model CPLW 1018, Zeiss Optical, Hannover Md) and was done following the mathematical model of Weibel. Differences between the groups were determined by one way ANOVA (p< 0.01).
Results: The VEGF was significantly decreased in the lungs of rats recovered in hyperoxia, it was correlated with a lower degree of alveolarization. Inhaled NO treatment after hyperoxia neither increase lung VEGF expression nor alveolarization.
Conclusion: The inhaled NO did not improve the changes observed in rat lungs after hyperoxia exposure.