摘要
作者通过记录大脑皮质体感诱发电位(SEP,)、光镜和电镜观察,研究了I-65对实验性鼠脑缺血和缺血后再灌流脑损伤的保护作用,结果显示:①对照组大鼠脑缺血再灌流时大脑皮质体感诱发电位明显抑制或完全抑制,光镜下皮质神经元胞体明显肿胀,细胞间隙增宽,尼氏体减少;电镜下神经细胞浆内粗面内质网(RER)明显减少.RER膜间隙扩张,严重者呈空泡状,线粒体肿胀明显,部分组粒体结构断裂,嵴消失,形成空泡.②给药组经I-65处理的大鼠脑缺血再灌流时大脑皮质体感诱发电位抑制程度较对照组明显减轻;光镜下神经细胞轻度肿胀,尼氏体减少不明显;电镜下神经细胞浆内RER丰富,排列整齐,线粒体轻度肿胀和嵴皱缩,未见明显的断裂现象.表明1-65对实验性鼠脑缺血和再灌流后的脑细胞机能与形态的完整性有明显的保护作用.
Intensive attention was recently payed to brain impairment due to acute cerebral ischemia and reperfusion, this paper reports on cortex somatosensory evoked potentials (SEPs), light microscope and electron microscope have been used to study the effect of calcium channel blocker I -65 on the brain impairment due to acute cerebral ischemia and reperfusion. The results suggest that 1-65 can protect electric activily of cerebral cortex neurons and ultrastructure of mitochondria and RER of neurons during acute cerebral ischemia and reperfusion. The mechanism may be blocking Ca2+ channel selectively so that preventing the increase of concentrations of Ca2+ within neurons.
出处
《中山医科大学学报》
CSCD
1991年第3期193-198,共6页
Academic Journal of Sun Yat-sen University of Medical Sciences
关键词
枸橼酸盐
脑缺血
大鼠
再灌注损伤
3,6-Dimethamidodibenzopyriodoniutn (I-65) Cerebral ischemia Cerebral reperfusion Cortex somatoensory evoked potentials Ultrastructure Rat