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N-acetylcysteine restores nitric oxide–mediated effects in the fetoplacental circulation of preeclamptic patients

2004; Elsevier BV; Volume: 191; Issue: 1 Linguagem: Inglês

10.1016/j.ajog.2003.12.033

1097-6868

Tanya M. Bisseling, Eva Maria Roes, Maarten T.M. Raijmakers, Eric A.P. Steegers, Wilbert H.M. Peters, Paul Smits,

Maternal and fetal healthcare

Objective Preeclampsia is associated with an imbalance between oxidants and antioxidants, resulting in reduced effects of the endothelium-derived, relaxing-factor nitric oxide (NO). Antioxidants, like N-acetylcysteine (NAC), remove reactive oxygen species, resulting in an improvement of endothelial function. We aimed to investigate the effect of NAC on the NO-pathway in the human fetoplacental circulation in preeclampsia and control pregnancies. Study design The NO-pathway was investigated by use of the NO-synthase inhibitor L-NAME in an ex vivo cotyledon perfusion model. Results At baseline, fetoplacental arterial pressure was comparable in preeclamptic pregnancies (n = 8) and control pregnancies (n = 8), and increased dose-dependently after L-NAME. The maximal L-NAME–induced rise in fetoplacental arterial pressure was attenuated in preeclamptic versus control pregnancies (20.8 ± 2.0 mm Hg vs 36.7 ± 3.5 mm Hg, P<.05). Addition of NAC increased the L-NAME–induced rise in fetoplacental arterial pressure to 36.4 ± 3.4 mm Hg in preeclampsia pregnancies (P<.05) and to 49.2 ± 2.6 mm Hg in control pregnancies (P<.05). Conclusion Preeclampsia is associated with a dysfunction of the NO-pathway. N-acetylcysteine increases NO-mediated effects in the fetoplacental circulation in preeclamptic placentas as well as in healthy control placentas.