期刊
ACTA NEUROLOGICA SCANDINAVICA
卷 111, 期 2, 页码 75-83出版社
WILEY
DOI: 10.1111/j.1600-0404.2004.00355.x
关键词
seizure; anti-epileptic drug; brain tumor; pathophysiology; treatment
Objective - The pathophysiological changes related to epileptic activity in peri- and intra-tumoral tissue are complex and have been only partly understood until now; possible mechanisms involve different structural, biochemical and histological tumor-related alterations. Methods - Medical databases were searched for evidence on influence of brain tumor-associated pH changes and hypoxia on epileptogenesis. Results - During the perioperative period, tumor-related hypoxia and acidity related to tumor neovascularization by vascular endothelial growth factor (VEGF) in combination with angiopoietins 1/2 (ang 1/2), may be a major factor contributing to outcomes involving epileptic activity after surgical tumor removal. Because anaerobic fermentation produces far less ATP than oxidative phosphorlyation per molecule of glucose, increased activity of the glycolytic pathway is necessary to maintain free ATP levels in the hypoxic cell. In mammalian cells, this metabolic switch is regulated by the transcription factor hypoxia-inducible factor-1. Conclusions - From the molecular point of view, therapeutic implications for the perioperative period may have relevance for the future.
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