BAY K-8644对大鼠脑全缺血致细胞毒性水肿的影响。

M Haida, Y Shinohara, M Yamamoto, T Nagayama, D Kurita
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引用次数: 0

摘要

钙通道激活剂BAY K-8644是一种二氢吡啶(DHP)衍生物,已被证明具有神经化学和行为活性,但其对缺血性脑损伤的影响尚不清楚。本报告描述了该药物对脑全缺血引起的细胞毒性水肿进展的影响,通过测量脑活检后1H-NMR松弛时间(T2)延长的时间常数k来评估。26雄性Wistar鼠被分成四组,(a)控制(生理盐水)组(n = 10), (b)湾k - 8644汽车组(n = 4), (c)湾k - 8644 0.03毫克/公斤组(n = 6)和(d)湾k - 8644 0.3毫克/公斤组(n = 6)。(d)的k值组,18.2 + / - 5.8分钟(平均+ / - SD),明显高于相比组(a) 10.3 + / - 1.6, 11.8 + / - 1.5 (b)和(c) 9.8 + / - 3.3分钟由方差分析(p < 0.01)。上述结果表明,BAY K-8644可延缓大鼠脑全缺血引起的细胞毒性水肿的进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The effect of BAY K-8644 on cytotoxic edema induced by total ischemia of rat brain.

The calcium channel activator BAY K-8644, a dihydropyridine (DHP) derivative, has been shown to possess neurochemical and behavioral activities, but its effect on ischemic brain damage has remained unknown. This report describes the effect of the drug on the progression of cytotoxic edema induced by total ischemia of the brain, evaluated by measuring the time constant, k, of elongation of the 1H-NMR relaxation time (T2) after brain biopsy. Twenty-six male Wistar rats were divided into four groups, (a) control (saline) group (n = 10), (b) BAY K-8644 vehicle group (n = 4), (c) BAY K-8644 0.03 mg/kg group (n = 6) and (d) BAY K-8644 0.3 mg/kg group (n = 6). The k value of group (d), 18.2 +/- 5.8 min (mean +/- SD), was significantly higher compared with those of groups (a) 10.3 +/- 1.6, (b) 11.8 +/- 1.5 and (c) 9.8 +/- 3.3 min (p < 0.01 by ANOVA). These results indicate that BAY K-8644 delayed the progression of cytotoxic edema induced by total ischemia of the rat brain.

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