应激性高血压大鼠海马CA1区在体外缺血的条件下形态结构和GM1的变化

Changes of Morphology and Monosialoganglioside Effects Following Ischemia in vitro on Stress-induced Hypertensive Rats Hippocampal Neurons in CA1 Sector

本实验观察了应激性高血压大鼠海马脑片在体外人工缺血条件下30,60,120min海马CAl区神经元形态结构的变化。同时观察了神经节苷脂GMl对其形态结构变化的影响。发现缺血30min神经元胞体变小,胞内小空泡形成,细胞器减少,少量的线粒体和内质网肿胀。核不规则,染色质分布不均,出现边集。随缺血时间的延长胞内大量细胞器破碎,残存细胞器结构不清,胞核固缩,部分裂解。神经节苷脂GMl(0.01％)具有明显的抗损害作用,减轻缺血所造成的上述形态学上的改变。

The neuropathological consequences of 'ischemia' 30, 60, 120 min and monosialogan-glioside effects were studied in CAl sector pyramidal neurons of hippocampal slice in vitro on stress-induced hypertensive rats. In the early stage of ischemia 30 min, the body of neurons became smaller. Vacuolation was found in cytoplasm and the number of organelle in CAl neuron sector decreased. Small amount mitochondria and endoplasmic reticula were dilatat-ed. Nuclei became irregularly and chromatic aggregated along the perinuclear membrane. In the late stage of ischemia 60 min to 120 min the structure of majority neurons became obscure, a part of them effractured. While with the drug treating during ischemia,the structure changes could be attenuated by GM1 (0. 01%). The results suggest that the GM1 might be more resistant to ischemia.