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RESEARCH PRODUCT
Prenatal Brain Damage in Preeclamptic Animal Model Induced by Gestational Nitric Oxide Synthase Inhibition
Sonia HerraizCarlos SimónAntonio LealB. PellicerAntonio Pellicersubject
medicine.medical_specialtyArticle SubjectPlacentaApoptosisBlood PressureBrain damagelcsh:Gynecology and obstetricsCrown-Rump LengthPre-EclampsiaPregnancyInternal medicinePlacentamedicineAnimalsRats WistarHypoxia Brainlcsh:RG1-991FetusPregnancyAnalysis of VarianceProteinuriabiologybusiness.industryObstetrics and GynecologyBrainOrgan SizeHypoxia (medical)medicine.diseaseRatsNitric oxide synthaseDisease Models AnimalFetal DiseasesEndocrinologymedicine.anatomical_structureNG-Nitroarginine Methyl Esterbiology.proteinGestationFemalemedicine.symptomNitric Oxide SynthasebusinessResearch Articledescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2010-09-15 |