TY - JOUR
T1 - N-acetylcysteine restores nitric oxide-mediated effects in the fetoplacentat circulation of preeclamptic patients
AU - Bisseling, T M
AU - Roes, E M
AU - Raijmakers, M T M
AU - Steegers, E A P
AU - Peters, W H M
AU - Smits, P
PY - 2004/7
Y1 - 2004/7
N2 - 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. (C) 2004 Elsevier Inc. All rights reserved.
AB - 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. (C) 2004 Elsevier Inc. All rights reserved.
UR - http://www.scopus.com/inward/record.url?scp=4043059412&partnerID=8YFLogxK
U2 - 10.1016/j.ajog.2003.12.033
DO - 10.1016/j.ajog.2003.12.033
M3 - Article
VL - 191
SP - 328
EP - 333
JO - American Journal of Obstetrics and Gynecology
JF - American Journal of Obstetrics and Gynecology
IS - 1
ER -