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- W2098706371 abstract "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." @default.
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- W2098706371 date "2004-07-01" @default.
- W2098706371 modified "2023-10-16" @default.
- W2098706371 title "N-acetylcysteine restores nitric oxide–mediated effects in the fetoplacental circulation of preeclamptic patients" @default.
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- W2098706371 doi "https://doi.org/10.1016/j.ajog.2003.12.033" @default.
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