Gilland E, Puka-Sundvall M, Andiné P, Bona E, Hagberg H
Department of Obstetrics and Gynecology, University of Göteborg, Sweden.
Brain Res Dev Brain Res. 1994 Nov 18;83(1):79-84. doi: 10.1016/0165-3806(94)90181-3.
In a model of perinatal hypoxia-ischemia (HI) we examined the neuroprotective efficacy of pre- and post-treatment with the glutamate release inhibitor BW1003C87 [5-(2,3,5-trichlorophenyl)-2,4-diamino-pyrimidine). Ipsilateral brain damage developed in 99% of rat pups subjected to HI (unilateral common carotid artery ligation and 100 min of 7.7% oxygen exposure) with a 26 +/- 16% (mean +/- S.D.) weight deficit of the damaged hemisphere 2 weeks after the insult. Pre-treatment with BW1003C87 (10 mg/kg intraperitoneally) reduced the brain damage by 46% (P < 0.05). A higher dose (20 mg/kg) of pre-treatment was not tolerated. Administration of BW1003C87 did not affect the rectal temperature of the rats. Post-treatment with BW1003C87 (10-30 mg/kg) offered no neuroprotection in this model. In conclusion, there was a neuroprotective effect from pre- but not post-treatment with BW1003C87 in this model, supporting the concept that intra-ischemic excitatory amino acid release is important for development of brain damage. The lack of post-treatment effect indicates that BW1003C87 did not attenuate deleterious EAA cycling during reflow in the neonatal brain.
在围产期缺氧缺血（HI）模型中，我们研究了用谷氨酸释放抑制剂BW1003C87[5-(2,3,5-三氯苯基)-2,4-二氨基嘧啶]进行预处理和后处理的神经保护效果。在接受HI（单侧颈总动脉结扎和100分钟7.7%氧气暴露）的大鼠幼崽中，99%出现同侧脑损伤，损伤后2周受损半球体重 deficit为26±16%（平均值±标准差）。用BW1003C87（10毫克/千克腹腔注射）预处理可使脑损伤减少46%（P<0.05）。更高剂量（20毫克/千克）的预处理无法耐受。给予BW1003C87不影响大鼠的直肠温度。在该模型中，用BW1003C87（10 - 30毫克/千克）进行后处理未提供神经保护作用。总之，在该模型中，BW1003C87预处理有神经保护作用，而后处理则没有，这支持了缺血时兴奋性氨基酸释放对脑损伤发展很重要的概念。后处理无效表明BW1003C87并未减弱新生脑再灌注期间有害的兴奋性氨基酸循环。 （注：原文中“weight deficit”表述不太准确，推测可能是“weight decrease”之类更准确表达体重减少的词，但按照要求未修改。）
