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背景:目前,形态学上地氟烷脑保护作用的证据尚不充足,机制还不清楚。目的:探讨地氟烷对全脑缺血再灌注损伤大鼠的脑保护作用及对凋亡和应激反应相关基因表达的影响。设计:以实验动物为研究对象,随机对照的实验研究。单位:一所大学医院的麻醉科和神经外科。材料:实验于2003-02/2004-02在首都医科大学附属北京神经外科研究所完成。成年雄性Wistar大鼠17只,随机分为缺血组7只、地氟烷组7只和假手术对照组3只。干预:制备大鼠全脑缺血再灌注模型。地氟烷组再灌注开始后立即吸入地氟烷1h。缺血组和地氟烷组每组取3只大鼠于再灌注1h(假手术组于手术后1h)取脑,利用电镜技术观察皮质超微结构的变化。缺血组和地氟烷组其余4只大鼠,利用基因芯片结合图像分析技术检测凋亡和应激反应相关基因的差异表达情况。主要观察指标:①皮质超微结构变化。②基因芯片检测凋亡和应激反应相关基因的差异表达情况。结果:与缺血组比较,地氟烷组神经元固缩少,神经元的细胞器和微管结构基本正常。与缺血组比较,地氟烷组凋亡蛋白酶激活因子下调。结论:地氟烷对神经元、细胞骨架可能具有保护作用,其机制可能与凋亡蛋白酶激活因子下调有关。
BACKGROUND: At present, there is not sufficient evidence for the protective effect of desflurane on morphology, and the mechanism is still unclear. Objective: To investigate the protective effects of desflurane on brain injury induced by global cerebral ischemia-reperfusion in rats and its effect on the expression of genes related to apoptosis and stress response. Design: Experimental animals as the research object, a randomized controlled experimental study. Unit: Anesthesiology and Neurosurgery at a university hospital. Materials: The experiment was performed at Beijing Institute of Neurosurgery, Capital Medical University from February 2003 to February 2004. Seventeen adult male Wistar rats were randomly divided into ischemia group (n = 7), desflurane group (n = 7) and sham operation control group (n = 3). Intervention: Preparation of rat global cerebral ischemia-reperfusion model. Desflurane inhaled desflurane immediately after reperfusion began 1h. The ischemic and desflurane groups were given 3 rats in each group for 1h after reperfusion (1h after operation in sham operation group). The changes of cortical ultrastructure were observed by electron microscopy. The remaining four rats in the ischemic group and the desflurane group were used to detect the differential expression of apoptosis-related and stress-related genes by gene chip and image analysis. MAIN OUTCOME MEASURES: ① cortical ultrastructure changes. ② Gene microarray detection of apoptosis and stress response related gene expression differences. Results: Compared with ischemic group, the neurons in desflurane group showed less pyknosis and contraction, and the organelles and microtubules in neurons were almost normal. Compared with ischemic group, the proteasome activator of desflurane group was down-regulated. CONCLUSION: Desflurane may have a protective effect on neurons and cytoskeleton, which may be related to the down-regulation of AP-activating factor.