N-acetylcysteine restores nitric oxide–mediated effects in the fetoplacental circulation of preeclamptic patients - 25/08/11
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.
Le texte complet de cet article est disponible en PDF.Keywords : Fetal placental vasculature, Preeclampsia, Nitric oxide, N-acetylcysteine, Cotyledon perfusion
Plan
 | Supported by grant no. 28-2801 from “Zorg Onderzoek Nederland,” The Hague, The Netherlands. T.M.B. and E.M.R. equally contributed to the manuscript. Reprints not available from the authors. |
Vol 191 - N° 1
P. 328-333 - juillet 2004 Retour au numéro
Article précédent
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