急性等容血液稀释对兔脑缺血再灌注神经细胞凋亡 s-100β蛋白及炎症因子的影响-effects of acute normovolemic hemodilution on apoptosis s - 100β protein and inflammatory factors in rabbit cerebral ischemia-reperfusion neurons.docxVIP

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急性等容血液稀释对兔脑缺血再灌注神经细胞凋亡 s-100β蛋白及炎症因子的影响-effects of acute normovolemic hemodilution on apoptosis s - 100β protein and inflammatory factors in rabbit cerebral ischemia-reperfusion neurons.docx

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急性等容血液稀释对兔脑缺血再灌注神经细胞凋亡 s-100β蛋白及炎症因子的影响-effects of acute normovolemic hemodilution on apoptosis s - 100β protein and inflammatory factors in rabbit cerebral ischemia-reperfusion neurons

Effect of acute normovolemic hemodilution on neuronal apoptosis and serum levels of S-100β protein and inflammatory cytokines in the cerebral ischemia reperfusionSpeciality：Anesthesiology Postgraduate：ZhengJinSupervisor：ProfessorHuang Huan-sen Department of Anesthesiology，the second affiliated hospital ofGuangzhou Medical UniversityABSTRACTBackgroundIn clinical, temporarily block parent artery in intracranial aneurysm surgery, regional brain tissue retraction in surgery, myocardial infarction, shock and respiratory and cardiac arrest can cause cerebral ischemia. Cerebral cells are extremely sensitive to ischemia. In order to avoid irreversible damage, timely restoration of cerebral blow flow is necessary. However, the restoration of cerebral blood flow can lead to the ischemia reperfusion injury. Cerebral ischemia reperfusion injury is triggered by a complex cascade of responses, including mitochondria damage, calcium overload, toxic effects of excitatory amino acids, free radicals generation, protease activation, apoptosis gene activation, inflammatory reactions and so on. All these responses reinforce each other, overlap, interrelate and create a vicious cycle ,eventually lead to apoptosis. A large number of studies have shown that cell apoptosis and cerebral ischemia reperfusion injury have a close relationship.Acute inflammatory reaction plays a key role in reperfusion induced secondary braininjury. In cerebral ischemia reperfusion, inflammatory cytokines and proenzymes activated by oxygen free radicals and other messengers induce the release of chemotactic factor, increase of adhesion molecule, and the interactions between leukocyte and endothelial cell. All the above result in leukocyte adhesion to vascular endothelial cell, then the microvascular obstruction happened following to a no-reflow phenomenon. Aggregation of cells release oxygen free radicals, proteolytic enzymes, cytokinins and so on , which directly injury endothelial cells leading to blood-bra