Abstract | OBJECTIVE: 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.
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Authors | Tanya M Bisseling, Eva Maria Roes, Maarten T M Raijmakers, Eric A P Steegers, Wilbert H M Peters, Paul Smits |
Journal | American journal of obstetrics and gynecology
(Am J Obstet Gynecol)
Vol. 191
Issue 1
Pg. 328-33
(Jul 2004)
ISSN: 0002-9378 [Print] United States |
PMID | 15295387
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Nitric Oxide
- Acetylcysteine
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Topics |
- Acetylcysteine
(pharmacology)
- Dose-Response Relationship, Drug
- Endothelium, Vascular
(drug effects)
- Female
- Humans
- In Vitro Techniques
- Nitric Oxide
(physiology)
- Placenta
(drug effects, physiology)
- Placental Circulation
(drug effects, physiology)
- Pre-Eclampsia
(physiopathology)
- Pregnancy
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