Abstract
We evaluated the effects of sustained perinatal inhibition of NO synthase (NOS) on hyperoxia induced lung injury in newborn rats. N(G)-nitro-L-arginine-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% O2 at 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 control us. 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.
Original language | English (US) |
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Pages (from-to) | 431-436 |
Number of pages | 6 |
Journal | Mediators of Inflammation |
Volume | 4 |
Issue number | 6 |
DOIs | |
State | Published - 1995 |
Keywords
- Antioxidant enzyme
- Hyperoxia
- N(G)-nitro-L-arginine-methyl-ester
- Nitric oxide
- Nitric oxide synthase
- Pulmonary artery
ASJC Scopus subject areas
- Immunology
- Cell Biology