Efeito neuroprotetor do anestésico propofol em fatias de hipocampo de ratos submetidos à isquemia cerebral in vitro

• Ano de defesa: 2009
• Autor(a) principal: Nancy Scardua Binda
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Farmacologia Bioquímica e Molecular; Anestésicos intravenosos; Propofol/farmacologia; Agentes neuroprotetores/farmacologia; Ratos Wistar; Neurofarmacologia; Propofol/uso terapêutico; Isquemia encefálica/induzido quimicamente; Canais de cálcio; In vitro
• Link de acesso: http://hdl.handle.net/1843/BUOS-8NHFYX

There are several studies that propofol, an intravenous anesthetic, reduces neuronal injury due to brain ischemia. However, the results of such neuroprotection in ischemic models have been conflicting, both in vitro and in vivo studies. In addition, the mechanisms involved in propofol neuroprotection have not been clarified. The aim of the present study was to investigate the neuroprotector effect of propofol in a model of brain ischemia in vitro, as well as probable mechanisms involved. To investigate the neuroprotector effect of propofol, we used the model hippocampus slices submitted to glucose and oxigen deprivation for 20 minutes. To assess the possible action locations of the anesthetic neuroprotection we used the following pharmacological tools: conotoxin MVIIC, N, -P/Q type calcium channel blockers, tetrodotoxin, a sodium channel blockers and EGTA, extracelular calcium quelator. In all concentrations assessed (1-300 M), propofol was able to reduce neuronal death in the CA1 region of the hippocampus. The maximum effect of propofol in neuronal death reduction (47,02%) was obtained with the concentration of 100 M. This effect seems to be dependent on the influx of Na+ through the Na+ ion channels sensible to voltage and extracellular Ca2+ influx. conotoxin MVIIC and propofol presented additional effects regarding neuroprotection, indicating that neuroprotetion by propofol could be independent of blocking voltage-dependent -N and -P/Q type Ca2+ channels. Therefore, this study suggests that propofol presents neuroprotector effects in hippocampus slices submitted to deprivation of glucose and oxigen. The mechanism of this neuroprotection seems to involve the reduction of the neuronal Na+ and Ca2+ influx independent of -N, -P/Q type Ca2+ channels.