Potter P E, Detwiler P, Thorne B, Moskal J R
Department of Anesthesiology, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, NY 10467.
Brain Res. 1991 Aug 30;558(1):127-30. doi: 10.1016/0006-8993(91)90728-e.
The ability of diphenylhydantoin (DPH) to prevent hypoxia-induced [3H]glutamate release was examined in perfused rat hippocampal slices. Hypoxia (25 min; 95% N2/5% CO2) caused a prolonged release of [3H]glutamate, which was reduced significantly if DPH (20 microM) was present from the beginning of the perfusion. Perfusion with oxygenated medium (reoxygenation) following hypoxia also caused a pronounced release of glutamate. A therapeutic concentration of DPH, added before, during, or after hypoxia, decreased this release of glutamate. These results suggest that DPH may protect against glutamate-mediated neurotoxicity associated with stroke.
在灌注的大鼠海马切片中检测了苯妥英（DPH）预防缺氧诱导的[3H]谷氨酸释放的能力。缺氧（25分钟；95%氮气/5%二氧化碳）导致[3H]谷氨酸的持续释放，如果从灌注开始就存在DPH（20微摩尔），则这种释放会显著减少。缺氧后用含氧培养基灌注（复氧）也会导致谷氨酸的明显释放。在缺氧前、缺氧期间或缺氧后添加治疗浓度的DPH，可减少谷氨酸的这种释放。这些结果表明，DPH可能预防与中风相关的谷氨酸介导的神经毒性。
