Yang C S, Tsai P J, Lin N N, Kuo J S
Department of Education and Research, Taichung Veterans General Hospital, Taiwan, ROC.
Chin J Physiol. 2000 Jun 30;43(2):49-53.
The effect of diethylmaleate administration on ascorbic acid release following cerebral ischemia was investigated in anesthetized rat brain cortex. Cerebral ischemia, induced by ligating bilateral common carotid arteries and unilateral middle cerebral artery, significantly increased the extracellular ascorbic acid levels. Diethylmaleate (4 mmoles/kg, i.p.), which has been shown in earlier studies to decrease the ischemia-induced glutamate release, significantly reduced the ischemia-induced ascorbic acid release. The ischemia-induced ascorbic acid release was unaffected by perfusing NMDA receptor antagonist MK 801 (75 microM). Additionally, elevated extracellular glutamate levels, achieved by either externally applied glutamate solutions or by perfusing L-trans-pyrrolidine-2,4-dicarboxylate (PDC) (31.4 mM and 15.7 mM) to inhibit the glutamate uptake transporter, also significantly increased the extracellular ascorbic acid levels. These results suggested that ascorbic acid release in cerebral ischemia might be related to the elevated extracellular glutamate levels, which occurs following cerebral ischemia.
在麻醉大鼠的大脑皮层中研究了顺丁烯二酸二乙酯给药对脑缺血后抗坏血酸释放的影响。通过结扎双侧颈总动脉和单侧大脑中动脉诱导的脑缺血显著增加了细胞外抗坏血酸水平。顺丁烯二酸二乙酯（4毫摩尔/千克，腹腔注射），在早期研究中已显示可减少缺血诱导的谷氨酸释放，显著降低了缺血诱导的抗坏血酸释放。缺血诱导的抗坏血酸释放不受灌注NMDA受体拮抗剂MK 801（75微摩尔）的影响。此外，通过外部施加谷氨酸溶液或灌注L-反式-吡咯烷-2,4-二羧酸（PDC）（31.4毫摩尔和15.7毫摩尔）以抑制谷氨酸摄取转运体来提高细胞外谷氨酸水平，也显著增加了细胞外抗坏血酸水平。这些结果表明，脑缺血时抗坏血酸的释放可能与脑缺血后细胞外谷氨酸水平升高有关。
