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stress induced hypertensive rat
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     Changes in the activity of Na+K+ -ATPase and GM1 effects were studied on the stress induced hypertensive rat et 3,12,and 24hours following occlusion of middle cerebral artery(MCAO). The decreases in the enzyme activity was observed in the three grops.
     采用SD大鼠,通过应激的方法制备高血压模型,并在此基础上阻断一侧大脑中动脉(MCAO),造成局灶性脑缺血。 观察了缺血后3、12、24h神经细胞膜Na+K+—ATPase活性的变化,同时观察了神经节苷脂GM1对其活性的影响。
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  相似匹配句对
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Changes in the activity of Na+K+ -ATPase and GM1 effects were studied on the stress induced hypertensive rat et 3,12,and 24hours following occlusion of middle cerebral artery(MCAO).The decreases in the enzyme activity was observed in the three grops.In the GM1 group,GM1(10mg/kg)was intraperitoneally injected 30 min. before occlusion,the decteases of Na+K+ -ATpase activity was signficantly attenuated in 3h group.It is suggested that the GM1 may protect function of cerebrum during the early phases of ischemic...

Changes in the activity of Na+K+ -ATPase and GM1 effects were studied on the stress induced hypertensive rat et 3,12,and 24hours following occlusion of middle cerebral artery(MCAO).The decreases in the enzyme activity was observed in the three grops.In the GM1 group,GM1(10mg/kg)was intraperitoneally injected 30 min. before occlusion,the decteases of Na+K+ -ATpase activity was signficantly attenuated in 3h group.It is suggested that the GM1 may protect function of cerebrum during the early phases of ischemic injury.

采用SD大鼠,通过应激的方法制备高血压模型,并在此基础上阻断一侧大脑中动脉(MCAO),造成局灶性脑缺血。观察了缺血后3、12、24h神经细胞膜Na+K+—ATPase活性的变化,同时观察了神经节苷脂GM1对其活性的影响。结果发现,随缺血时间的延长酶活性逐渐降低,GM1术前30min给药(10mg/kg)能明显抑制缺血后3h酶活性的下降,但对缺血后12、24h酶活性的下降无改善作用。提示GM1术前给药对缺血早期具有脑保护作用。

The effect of GM1 antagonist Cholera-Toxin on the changes of neuronal morphology in the hippocampal slice CA1 sector of stress-induced hypertensive rats were studied after"ischemia" 30,60,120min.In the early stage of ischemia 30min,that the body of neurons became smaller;shape irregular and cell detaching each other.Nuclei of affected neurons were pyknotic.Time-dependent morphological changes became more obvious from 60min to 120min.The number of neuron in CA1 sector decreased.Ultrastructural...

The effect of GM1 antagonist Cholera-Toxin on the changes of neuronal morphology in the hippocampal slice CA1 sector of stress-induced hypertensive rats were studied after"ischemia" 30,60,120min.In the early stage of ischemia 30min,that the body of neurons became smaller;shape irregular and cell detaching each other.Nuclei of affected neurons were pyknotic.Time-dependent morphological changes became more obvious from 60min to 120min.The number of neuron in CA1 sector decreased.Ultrastructural examination showed that majority of microvacuoles in the neuronal cytoplasm correspond to swollen mitochondria.Both smooth and granular endoplasmic reticula were dilatated.Nuclei became irregularly and chromatic aggregated along the perinuclear membrane.In the late stage of ischemia 60min to 120min the structure of neurons became obscure,a part of them reptured.There occured macrovaculation in cytoplasm and nucler shrank.While with the drug treating during ischemia,the structure of injured neuron could be exacerbated by GM1 antagonist Cholera-Toxin(0.001%).

实验观察了神经节苷脂GM1拮抗剂——霍乱毒素对应激性高血压大鼠海马脑片体外人工缺血30、60、120minCA1区神经元形态结构的影响。缺血30min时胞体变小,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细胞器破碎,残存细胞器结构不清,胞核固缩,部分裂解。而霍乱毒素则加重缺血30、60、120minCA1区神经元形态学上的改变,具有明显的神经元损害作用。

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...

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.

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。

 
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