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Emulsified isoflurane anesthesia decreases brain-derived neurotrophic factor expression and induces cognitive dysfunction in adult rats

Post-operative cognitive dysfunction (POCD) is a severe complication characterized by cognitive decline in patients following anesthesia and surgery. Previous studies have suggested that volatile anesthetics, for example isoflurane, may contribute to such impairment. In the present study, the effect...

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Detalles Bibliográficos
Autores principales: ZHANG, FAN, ZHU, ZHAO-QIONG, LIU, DE-XING, ZHANG, CHAO, GONG, QI-HAI, ZHU, YU-HANG
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4079394/
https://www.ncbi.nlm.nih.gov/pubmed/25009603
http://dx.doi.org/10.3892/etm.2014.1769
Descripción
Sumario:Post-operative cognitive dysfunction (POCD) is a severe complication characterized by cognitive decline in patients following anesthesia and surgery. Previous studies have suggested that volatile anesthetics, for example isoflurane, may contribute to such impairment. In the present study, the effects of emulsified isoflurane (EI) exposure on cognitive function, as well as the potential mechanisms, were investigated in animal models. Eight-month-old male rats were administered a single intravenous injection of 8% EI. The rats were then subjected to the Morris water maze test to assess their cognitive functions at different time-points following drug administration. Samples were taken in order to detect the plasma corticosterone concentration and the levels of hippocampal brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), as well as the expression of BDNF and NGF in the hippocampal region. The results showed that a single injection of EI caused reversible learning and memory dysfunction in adult rats. It was found that downregulation of BDNF expression may contribute to the isoflurane-induced cognitive impairment of these rats. Increased expression of NGF may be associated with the protection mechanism subsequent to learning and memory function decline, and therefore may accelerate the recovery of cognitive function.