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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

Systolic blood pressure evolution in pregnant rat. Control group shows levels that remain constant along pregnancy except day 10, when SBP falls, like in human pregnancies. L-NAME group showed an increase in SBP values in pregnancy, which was significant from day 6. (E6 P < .05; E10 P < .0001; E18 P < .05).
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fig1: Systolic blood pressure evolution in pregnant rat. Control group shows levels that remain constant along pregnancy except day 10, when SBP falls, like in human pregnancies. L-NAME group showed an increase in SBP values in pregnancy, which was significant from day 6. (E6 P < .05; E10 P < .0001; E18 P < .05).

Mentions: SBP showed a significant increase in the L-NAME group in all the evaluated moments throughout the pregnancy when compared with the control group, as shown in Figure 1, and this significance was clear since day 6 of pregnancy (E6 P < .05, E11 P < .0001 and E18 P < .05) Also, it showed the presence of proteinuria.


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)

Systolic blood pressure evolution in pregnant rat. Control group shows levels that remain constant along pregnancy except day 10, when SBP falls, like in human pregnancies. L-NAME group showed an increase in SBP values in pregnancy, which was significant from day 6. (E6 P < .05; E10 P < .0001; E18 P < .05).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Systolic blood pressure evolution in pregnant rat. Control group shows levels that remain constant along pregnancy except day 10, when SBP falls, like in human pregnancies. L-NAME group showed an increase in SBP values in pregnancy, which was significant from day 6. (E6 P < .05; E10 P < .0001; E18 P < .05).
Mentions: SBP showed a significant increase in the L-NAME group in all the evaluated moments throughout the pregnancy when compared with the control group, as shown in Figure 1, and this significance was clear since day 6 of pregnancy (E6 P < .05, E11 P < .0001 and E18 P < .05) Also, it showed the presence of proteinuria.

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