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一氧化氮合酶抑制剂对缺血性海马迟发性神经元死亡的保护作用 被引量:1
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作者 王汉 黄怀钧 王凤霞 《卒中与神经疾病》 1999年第3期137-139,共3页
目的 :研究一氧化氮 ( NO)在缺血性海马迟发性神经元死亡 ( DND)中的作用 ,观察非选择性一氧化氮合酶 ( nitricoxidesynthase,NOS)抑制剂 NG-nitro-L-arginine( L-NNA)对缺血性海马 DND的影响。方法 :实验分为假手术组、生理盐水治疗组... 目的 :研究一氧化氮 ( NO)在缺血性海马迟发性神经元死亡 ( DND)中的作用 ,观察非选择性一氧化氮合酶 ( nitricoxidesynthase,NOS)抑制剂 NG-nitro-L-arginine( L-NNA)对缺血性海马 DND的影响。方法 :实验分为假手术组、生理盐水治疗组、L-NNA治疗组。采用大鼠 4血管关闭方法制作了全脑缺血再灌流模型 ,以假手术组为对照 ,检测了脑缺血 1 0 min再灌流 72 h海马区 NOS活性的变化并观察计量了海马 CA1 区组织病理改变 ;同时观察了 L-NNA对海马区 NOS活性和 CA1 区病理改变的影响。结果 :生理盐水治疗组海马组织 NOS活性显著升高( P<0 .0 1 ) ,L-NNA可部分抑制海马区 NOS活性 ( P<0 .0 1 ) ,使海马 CA1 区神经元存活数显著增加 ( P<0 .0 1 )。结论 :NO在海马 CA1 区 DND发生中具有毒性作用 ,L-NNA对海马 CA1 区神经元损伤有一定的保护作用。 展开更多
关键词 一氧化氮 迟发性 神经元死亡 缺血性海马
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EFFECT OF VASOPRESSIN ON DELAYED NEURONALDAMAGE IN HIPPOCAMPUS FOLLOWING CEREBRALISCHEMIA AND REPERFUSION IN GERBILS
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作者 刘新峰 金泳清 陈光辉 《Chinese Medical Sciences Journal》 CAS CSCD 1996年第2期93-96,共4页
Mongolian gerbils were used as delayed neuronal damage (DNDi animal models. At the end of 15Abstract:Mongolian gerbils were used as delayed neuronal damage (DND)animal models. At the end of 15 minute cerebral ischemi... Mongolian gerbils were used as delayed neuronal damage (DNDi animal models. At the end of 15Abstract:Mongolian gerbils were used as delayed neuronal damage (DND)animal models. At the end of 15 minute cerebral ischemia and at various reperfusion time ranging from 1 to 96 hours, the content of water and arginine vasopressin (AVP) in the CA1 sector of hippocampus were measured by the specific gravity method and radioimmunoassay. Furthermore, we also examined the effect of intracerebroventricular (ICV) injection of AVP, AVP antiserum on calcium, Na+, K+-ATPase activrty in the CA1 sector after ischemia and 96 hour reperfusion. The results showed that AVP contents of CA1 sector of hippocampus during 6 to 96 hour recirculation, and the water content of CA1 sector during 24 to 96 hour were significantly and continuously increased. After ICV inJection of AVP, the water content and calcium in CA1 sector of hippocampus at cerebral ischemia and 96 hour recirculation further increased, and the Na+, K+- ATPase activity in CA1 sector was remarkably decreased as compared with that of control. While ICV injection of AVP antiserum, the water content and calcium in CA1 sector were significantly decreased as com pared with that of control. These suggested that AVP was involved in the pathophysiologic process of DND in hippocampus following cerebral ischemia and reperfusion. Its mechanism might be through the change of intracellular action mediated by specific AVP receptor to lead to Ca ions over-load of neuron and inhibit the Na+, K+- ATPase activity , thereby to exacerbate the DND in hippocampus. 展开更多
关键词 cerebal ischemia VASOPRESSIN HIPPOCAMPUS
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