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Prenatal brain damage in preeclamptic animal model induced by gestational nitric oxide synthase inhibition.

Pellicer B, Herraiz S, Leal A, Simón C, Pellicer A - J Pregnancy (2010)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Servicio Ginecologia y Obstetricia, Hospital de Manises, C/Roses S/N, 46940 Valencia, Spain. pellicer_beg@gva.es

ABSTRACT
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.

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Related in: MedlinePlus

Analysis of apoptotic activity in fetal brain. A-pallidum zone (P = .0028). B-subventricular zone (P = .0024). C-striatum (P = .03).
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fig6: Analysis of apoptotic activity in fetal brain. A-pallidum zone (P = .0028). B-subventricular zone (P = .0024). C-striatum (P = .03).

Mentions: L-NAME group showed an increased pattern of apoptotic activity of the fetal brain versus the control group (P < .05, Figure 5). When we analysed specific cerebral areas, we found that in the pallidum zone of the fetal brain there was a significant increase in the apoptotic activity detected as compared to the control group (P = .0028) (Figure 6(a)). In the subventricular zone there was also a significant increase in the apoptotic activity (P = .0024) (Figure 6(b)).


Prenatal brain damage in preeclamptic animal model induced by gestational nitric oxide synthase inhibition.

Pellicer B, Herraiz S, Leal A, Simón C, Pellicer A - J Pregnancy (2010)

Analysis of apoptotic activity in fetal brain. A-pallidum zone (P = .0028). B-subventricular zone (P = .0024). C-striatum (P = .03).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3066555&req=5

fig6: Analysis of apoptotic activity in fetal brain. A-pallidum zone (P = .0028). B-subventricular zone (P = .0024). C-striatum (P = .03).
Mentions: L-NAME group showed an increased pattern of apoptotic activity of the fetal brain versus the control group (P < .05, Figure 5). When we analysed specific cerebral areas, we found that in the pallidum zone of the fetal brain there was a significant increase in the apoptotic activity detected as compared to the control group (P = .0028) (Figure 6(a)). In the subventricular zone there was also a significant increase in the apoptotic activity (P = .0024) (Figure 6(b)).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Servicio Ginecologia y Obstetricia, Hospital de Manises, C/Roses S/N, 46940 Valencia, Spain. pellicer_beg@gva.es

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus