Impact of neonatal anoxia and hypothermic treatment on development and memory of rats.

Therapeutic hypothermia (TH) is well established as a standard treatment for term and near-term infants. However, therapeutic effects of hypothermia following neonatal anoxia in very premature babies remains inconclusive. The present rodent model of preterm neonatal anoxia has been shown to alter developmental milestones and hippocampal neurogenesis, and to disrupt spatial learning and memory in adulthood. These effects seem to be reduced by post-insult hypothermia. Epigenetic-related mechanisms have been postulated as valuable tools for developing new therapies. Dentate gyrus neurogenesis is regulated by epigenetic factors. This study evaluated whether TH effects in a rodent model of preterm oxygen deprivation are based on epigenetic alterations. The effects of TH on both developmental features (somatic growth, maturation of physical characteristics and early neurological reflexes) and performance of behavioral tasks at adulthood (spatial reference and working memory, and fear conditioning) were investigated in association with the possible involvement of the epigenetic operator Enhancer of zeste homolog 2 (Ezh2), possibly related to long-lasting effects on hippocampal neurogenesis. Results showed that TH reduced both anoxia-induced hippocampal neurodegeneration and anoxia-induced impairments on risk assessment behavior, acquisition of spatial memory, and extinction of auditory and contextual fear conditioning. In contrast, TH did not prevent developmental alterations caused by neonatal anoxia and did not restore hippocampal neurogenesis or cause changes in EZH2 levels. In conclusion, despite the beneficial effects of TH in hippocampal neurodegeneration and in reversing disruption of performance of behavioral tasks following oxygen deprivation in prematurity, these effects seem not related to developmental alterations and hippocampal neurogenesis and, apparently, is not caused by Ezh2-mediated epigenetic alteration.

Protein ubiquitination in postsynaptic densities after hypoxia in rat neostriatum is blocked by hypothermia.

Synaptic dysfunction has been associated with neuronal cell death following hypoxia. The lack of knowledge on the mechanisms underlying this dysfunction prompted us to investigate the morphological changes in the postsynaptic densities (PSDs) induced by hypoxia. The results presented here demonstrate that PSDs of the rat neostriatum are highly modified and ubiquitinated 6 months after induction of hypoxia in a model of perinatal asphyxia. Using both two dimensional (2D) and three dimensional (3D) electron microscopic analyses of synapses stained with ethanolic phosphotungstic acid (E-PTA), we observed an increment of PSD thickness dependent on the duration and severity of the hypoxic insult. The PSDs showed clear signs of damage and intense staining for ubiquitin. These morphological and molecular changes were effectively blocked by hypothermia treatment, one of the most effective strategies for hypoxia-induced brain injury available today. Our data suggest that synaptic dysfunction following hypoxia may be caused by long-term misfolding and aggregation of proteins in the PSD.

Aspectos relevantes de la encefalopatía hipóxico-isquémica / Hypoxic-ischemic encephalopaty aspects relevants

El seguimiento del embarazo, la atención del parto y la reanimación del recién nacido, exigen la detección oportuna y el tratamiento adecuado del sufrimiento cerebral debido a la asfixia. Una vez que la lesión cerebral se establece, todos los esfuerzos estarán encaminados a disminuir sus consecuencias. La coordinación entre el obstetra y el pediatra, fundada en la confianza mutua, el profesionalismo y la experiencia de ambos favorece la toma de decisiones pertinentes, para otorgar al niño la posibilidad de preservar, en lo posible su evolución motora e intelectual

Estudo dos fatores de risco desencadeantes de anóxia neonatal e o possível desenvolvimento de paralisia cerebral / Study of risk factors that unchain newborn anoxy and the possible development of cerebral palsy

A proposta deste estudo foi identificar os fatores de risco desencadeantes de anóxia neonatal e o possível desenvolvimento de Paralisia Cerebral. A coleta dos dados foi realizada a partir de informaçöes contidas no Serviço Arquivo Médico (SAME) do Hospital Universitário de Santa Maria (UFSM), RS. Participaram deste estudo crianças atendidadas na UTI neonatal do HUSM durante o ano de 1988, com diagnóstico de anóxia neonatal. Os 59 casos encontrados foram classificados em grupos de recuperaçäo total e recuperaçäo parcial. Sendo submetidos a análise descritiva. Os resultados encontram suporte na literatura onde a anóxia neonatal é considerada como uma das principais causas de paralisia cerebral, confirmando a necessidade de acompanhamento destas crianças até a idade escolar

Complicaciones neurológicas en pacientes sometidos a cirugía cardiovascular / Neurological complications following cardiac surgery

Las complicaciones neurologícas ocupan un lugar importante en cirugía cardiovascular dado que los trastornos orgánicos, sociales y económicos que originan influyen en el ámbito médico familiar. A pesar del avance en la tecnología aplicada a aparatos y sistemas médicos empleados durante la misma, no ha sido posible abolirlas, influyendo en esto el factor humano y técnico, así como la presencia previa de patología orgánica; pudiendo precipitar la incidencia de éstas al romperse el equilibrio fisiologíco cerebral, manifestado clínicamente por una gran variedad de signos y síntomas que el médico anestesiólogo debe identificar oportunamente, para instalar el tratamiento adecuado inicial apoyado por otros servicios médicos especializados necesarios y así disminuir la morbimortalidad y secuelas de estas complicaciones.