Effect of high dose NOS inhibitor on neurone apoptosis in focal cerebral ischemia
Xiao Lu
Abstract
Xiao Lu
Abstract
ObjectiveTo study the relationship between nitric oxide (NO) and apoptosis in the focal cerebral ischemia. MethodsUsing light microscope and electric microscope,the pathological changes of cerebral in the focal cerebral ischemia were observed. ResultsWhen the focal cerebral ischemia in rats was influenced by high dose N nitro L arginine ( NNLA ), the operation side brain appeared edema around nucleus, dissolutuin and distortion of neuronal cell nucleus in a part of hippocampus CA4 region and cortex region. These changes under hight microscope were more obvious than that in operation control group. Under electric microscope, the changes of the organelles of neuronal cell nucleus and chromatin dense stain of gliocyte nucleus in ischemic penumbra were found. ConclusionExcessive NO has two forms to induce neuron injury. First,excessive NO is a reactive oxygen species (ROS). It may attack straightly to nerves and vascular endothelial cell and is a direct toxicity molecule. Second, the lack of NO can not keep the cerebrovasurlar basic tension. It may induce the decrease of cerebral blood flow and anoxia and neuron injury.
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ObjectiveTo study the relationship between nitric oxide (NO) and apoptosis in the focal cerebral ischemia. MethodsUsing light microscope and electric microscope,the pathological changes of cerebral in the focal cerebral ischemia were observed. ResultsWhen the focal cerebral ischemia in rats was influenced by high dose N nitro L arginine ( NNLA ), the operation side brain appeared edema around nucleus, dissolutuin and distortion of neuronal cell nucleus in a part of hippocampus CA4 region and cortex region. These changes under hight microscope were more obvious than that in operation control group. Under electric microscope, the changes of the organelles of neuronal cell nucleus and chromatin dense stain of gliocyte nucleus in ischemic penumbra were found. ConclusionExcessive NO has two forms to induce neuron injury. First,excessive NO is a reactive oxygen species (ROS). It may attack straightly to nerves and vascular endothelial cell and is a direct toxicity molecule. Second, the lack of NO can not keep the cerebrovasurlar basic tension. It may induce the decrease of cerebral blood flow and anoxia and neuron injury.
Key concepts: Penumbra, Ischemia, Cerebral cortex, Nucleus, Pathology, Medicine, Anatomy, Biology