Nitric oxide synthase inhibition decreases tolerance to hyperoxia in newborn rats

M. R. Pierce ； C. A. Voelker ； I. R. S. Sosenko ； S. Bustamante ； S. M. Olister ； X.-J. Zhang ； D. A. Clark ； M. J. S. Miller

《Mediators of Inflammation》 1995卷 (1995/12) Pp. 431-436

https://doi.org/10.1155/S096293519500069X

摘要

WE evaluated the effects of sustained perinatal inhibition of NO synthase (NOS) on hyperoxia induced lung injury in newborn rats. N^G-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% O_2) or room air. The survival rate of L-NAME treated pups when placed in ＞ 95% O_2 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 vs. 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.

關鍵字

Antioxidant enzyme ； hyperoxia ； N^G-nitro-Larginine-methyl-esterlnitric oxidelnitric oxide synthase ； pulmonary artery