Why the study?
Does chronic administration of a nitric oxide synthase inhibitor (L-NAME) induce prenatal brain damage in an animal model of preeclampsia?
Does chronic administration of a nitric oxide synthase inhibitor (L-NAME) induce prenatal brain damage in an animal model of preeclampsia?
Chronic hypoxia induced by L-NAME in a preeclamptic animal model increases apoptotic activity in fetal brains, particularly in the subventricular and pallidum zones, potentially explaining clinical features of cerebral palsy.
Links preeclampsia hypoxia to regional fetal brain apoptosis in animal models; hypothesis-generating for cerebral palsy mechanisms, no practice change.
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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Pellicer et al. (2010) studied this question.
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