Kano T, Katayama Y, Miyazaki S, Kinoshita K, Kawamata T, Tsubokawa T
Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan.
Neuropharmacology. 1993 Mar;32(3):307-10. doi: 10.1016/0028-3908(93)90117-l.
The effects of indeloxazine on the ischemia-induced death of hippocampal CA1 pyramidal cells following transient cerebral ischemia were examined in the mongolian gerbil. Increased survival of CA1 pyramidal cells was demonstrated in animals pre- and post-treated with indeloxazine. Increased survival of CA1 pyramidal cells was, however, not demonstrated in animals post-treated but not pre-treated with indeloxazine. A previous study has demonstrated that indeloxazine increases the glucose and adenosine triphosphate (ATP) contents in the brain probably through an enhanced capability of oxidative phosphorylation. It has been reported that increases in the glucose and ATP contents in the brain before ischemia delay the onset of massive ionic fluxes during ischemia. The delay in onset of this ionic event may help to protect these cells from death. The present data suggest that energy state before ischemia may play an important role in the protective effect of indeloxazine.
在蒙古沙土鼠中研究了茚达品对短暂性脑缺血后海马CA1锥体神经元缺血性死亡的影响。预先和事后用茚达品处理的动物中，CA1锥体神经元的存活率增加。然而，事后但未预先用茚达品处理的动物中，未观察到CA1锥体神经元存活率增加。先前的一项研究表明，茚达品可能通过增强氧化磷酸化能力来增加脑中葡萄糖和三磷酸腺苷（ATP）的含量。据报道，缺血前脑中葡萄糖和ATP含量的增加会延迟缺血期间大量离子通量的发生。这种离子事件发生时间的延迟可能有助于保护这些细胞免于死亡。目前的数据表明，缺血前的能量状态可能在茚达品的保护作用中起重要作用。
