Nitric oxide synthase inhibition decreases tolerance to hyperoxia in newborn rats

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

doi:10.1155/S096293519500069X

Nitric oxide synthase inhibition decreases tolerance to hyperoxia in newborn rats

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

Pediatrics

Research output: Contribution to journal › Article

11 Scopus citations

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)
Pages (from-to)	431-436
Number of pages	6
Journal	Mediators of Inflammation
Volume	4
Issue number	6
DOIs	https://doi.org/10.1155/S096293519500069X
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

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Pierce, M. R., Voelker, C. A., Bustamante, S., Olister, S. M., Zhang, X. J., Clark, D. A., Miller, M. J. S., & Sosenko, I. R. S. (1995). Nitric oxide synthase inhibition decreases tolerance to hyperoxia in newborn rats. Mediators of Inflammation, 4(6), 431-436. https://doi.org/10.1155/S096293519500069X

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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.",

keywords = "Antioxidant enzyme, Hyperoxia, N(G)-nitro-L-arginine-methyl-ester, Nitric oxide, Nitric oxide synthase, Pulmonary artery",

author = "Pierce, {M. R.} and Voelker, {C. A.} and S. Bustamante and Olister, {S. M.} and Zhang, {X. J.} and Clark, {D. A.} and Miller, {M. J.S.} and Sosenko, {I. R.S.}",

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AU - Pierce, M. R.

AU - Voelker, C. A.

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AU - Zhang, X. J.

AU - Clark, D. A.

AU - Miller, M. J.S.

AU - Sosenko, I. R.S.

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N2 - 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.

AB - 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.

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KW - Nitric oxide synthase

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