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Human Reproduction, Vol. 15, No. 8, 1838-1842, August 2000
© 2000 European Society of Human Reproduction and Embryology

Inhibition of nitric oxide synthesis causes preterm delivery in the mouse

Gian Mario Tiboni1 and Franca Giampietro

Sezione di Ostetricia e Ginecologia, Dipartimento di Medicina e Scienze dell'Invecchiamento, Facoltà di Medicina e Chirurgia, Università `G. d'Annunzio', Chieti, Italy

The aim of the present study was to investigate whether an inhibitor of nitric oxide (NO) synthesis provokes preterm delivery in a mouse model. ICR (CD-1) mice were injected s.c. with NG-nitro-L-arginine methyl esther (L-NAME) at 0, 40, 70 or 100 mg/kg on gestation day (GD) 15.5 and 16. Delivery was considered preterm if it occurred before GD 18. In a satellite study, the potential ability of the NO donor sodium nitroprusside (SNP) to prevent L-NAME-induced preterm delivery was tested. Five hours before the initiation of treatment regimen with L-NAME at 70 mg/kg, mice were implanted s.c. with micro-osmotic pumps infusing SNP at 0 or 10 µg/kg/min continuously for 3 days. Administration of L-NAME evoked preterm delivery. This response was noted in 64 and 60% of animals treated with 70 and 100 mg/kg L-NAME respectively (P < 0.05 versus control value). Infusion with SNP provided complete and significant (P < 0.05 versus positive control value) protection from L-NAME-initiated preterm delivery. This is the first report to reveal that an inhibitor of NO synthesis initiates preterm delivery in a mouse model.

Key words: L-NAME/mouse /nitric oxide/preterm delivery

1 To whom correspondence should be addressed at: Sezione di Ostetricia e Ginecologia, Dipartimento di Medicina e Scienze dell'Invecchiamento, Facoltà di Medicina e Chirurgia, Università `G. d'Annunzio', Presidio Ospedaliero SS. Annunziata, Colle dell'Ara, 66100, Chieti, Italy. E-mail: tiboni{at}unich.it


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[Abstract] [PDF]


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