Prenatal Brain Damage in Preeclamptic Animal Model Induced by Gestational Nitric Oxide Synthase Inhibition

Cerebral palsy is a major neonatal handicap with unknown aetiology. There is evidence that prenatal brain injury is the leading cause of CP. Severe placental pathology accounts for a high percentage of cases. Several factors predispose to prenatal brain damage but when and how they act is unclear. T...

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Bibliographic Details
Published in:Journal of Pregnancy 2011-01, Vol.2011 (2011), p.255-260
Main Authors: Pellicer, Begoña, Herraiz, Sonia, Leal, Antonio, Simón, Carlos, Pellicer, Antonio
Format: Article
Language:English
Subjects:
Analysis of Variance
Animals
Apoptosis
Blood Pressure
Brain - pathology
Crown-Rump Length
Disease Models, Animal
Female
Fetal Diseases - etiology
Fetal Diseases - pathology
Hypoxia, Brain - embryology
Hypoxia, Brain - etiology
Hypoxia, Brain - pathology
NG-Nitroarginine Methyl Ester
Nitric Oxide Synthase - antagonists & inhibitors
Organ Size
Placenta - pathology
Pre-Eclampsia - chemically induced
Pre-Eclampsia - physiopathology
Pregnancy
Rats
Rats, Wistar
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Summary:Cerebral palsy is a major neonatal handicap with unknown aetiology. There is evidence that prenatal brain injury is the leading cause of CP. Severe placental pathology accounts for a high percentage of cases. Several factors predispose to prenatal brain damage but when and how they act is unclear. The aim of this paper was to determine if hypoxia during pregnancy leads to damage in fetal brain and to evaluate the localization of this injury. An animal model of chronic hypoxia produced by chronic administration of a nitric oxide synthase inhibitor (L-NAME) was used to evaluate apoptotic activity in fetal brains and to localize the most sensitive areas. L-NAME reproduces a preeclamptic-like condition with increased blood pressure, proteinuria, growth restriction and intrauterine mortality. Apoptotic activity was increased in L-NAME brains and the most sensitive areas were the subventricular and pallidum zone. These results may explain the clinical features of CP. Further studies are needed.
ISSN:2090-2727
2090-2735
DOI:10.1155/2011/809569