论文部分内容阅读
目的 探讨纳洛酮对全脑缺血再灌注损伤的防治作用及其机理。方法 96只大鼠随机分为对照组、损伤组和纳洛酮治疗组。采用四血管阻断模型 ,动态测定脑组织及血浆 β -内啡肽 (β -EP)、脑组织总钙和脑组织超氧化物歧化酶(SOD)活性、丙二醛 (MDA)浓度、脑组织水含量及海马CA1区神经元记数的变化。结果 随再灌注时间的延长 ,脑组织 β -EP水平显著增高 ,而血浆的变化滞后于脑组织的变化 ,脑组织总钙水平、MDA浓度、脑组织水含量显著增高 ,脑组织SOD活性及海马CA1区神经元记数显著降低 (P <0 0 5和P <0 0 1)。使用纳洛酮后上述各指标的异常变化明显减轻 ,与损伤组比有显著性差异 (P <0 0 5和P <0 0 1)。结论 纳洛酮可减轻全脑缺血再灌注损伤 ,其机制与拮抗 β -EP活性、降低脑组织总钙和氧自由基水平有关
Objective To investigate the preventive and therapeutic effects of naloxone on global cerebral ischemia-reperfusion injury and its mechanism. Methods 96 rats were randomly divided into control group, injury group and naloxone treatment group. The four - vessel occlusion model was used to measure the activity of brain tissue, β - endorphin (β - EP), the content of total calcium and brain tissue superoxide dismutase (SOD), malondialdehyde (MDA) Changes of Tissue Water Content and Neuron Count of Hippocampal CA1 Region. Results With the prolongation of reperfusion time, the level of β-EP in brain tissue was significantly increased, while the changes of plasma lagged behind in brain tissue. The levels of total calcium, MDA, brain water content, brain SOD activity and hippocampus Neuron counts in CA1 area decreased significantly (P <0 05 and P 0 01). Naloxone after use of the above indicators of abnormal changes significantly reduced, compared with the injury group was significantly different (P <0 05 and P 0 01). Conclusion Naloxone can reduce the global cerebral ischemia-reperfusion injury, and its mechanism is related to the antagonism of β-EP activity and the decrease of total calcium and oxygen free radicals in brain tissue