摘要
目的 探讨GM1对脑缺血再灌注损伤的神经细胞的保护作用。方法 仿照Pulsinelli四血管闭塞法建立大鼠全脑缺血再灌注损伤模型 ,观测外源性GM1对脑缺血再灌注损伤后脑细胞外液乳酸及葡萄糖含量的影响。结果 :急性缺血再灌注组、GM1治疗组乳酸缺血后迅速升高 ,再灌注 30min达高峰 ,其后逐渐下降。再灌注组在 30～ 12 0min内显著高于对照组 ,治疗组在 30～ 90min内显著高于对照组 ,但低于再灌注组 (P <0 0 5 )。急性缺血再灌注组、GM1治疗组葡萄糖缺血后迅速降低 ,再灌注 30min达低谷 ,其后逐渐上升。再灌注组在 30～ 12 0min内显著低于对照组 ,治疗组在30 90min内低于对照组 ,但显著高于再灌注组 (P <0 0 5 )。结论 脑缺血再灌注损伤后 ,早期使用GM1治疗 ,明显减轻脑组织中乳酸的堆积 ,增加葡萄糖含量 ,增强神经元细胞的存活 ,为探索GM1在脑缺血再灌注后的神经保护提供了新的途径。
Objective To investigate the neuroprojective effects of GM1 on rat global cerebral ischemic reperfusion damage.Methods Pulsinelli’s method was employed to establish cerebral ischemia reperfusion animal model.The dynamic varieties of lactate and glucose were observed after giving exogenous GM1.Results Baseline levels of lactate in acute ischemia and reperfusion group and GM1 group were the same as sham group's. They increased swiftly after lack of blood, and reached the peak 30 min after the brain reperfusion, then gradually fell. The levels in acute ischemia and reperfusion group were notably higher than sham group’s in 30～120 min. The levels in GM1 group were notably higher than sham group’s, but lower than acute ischemia and reperfusion group’s in 30～90 min(P<0.05). Baseline level of glucose in acute ischemia and reperfusion group and GM1 group was the same as sham group’s. It fell swiftly after lack of blood, and reached peak 30 min after brain reperfusion, then gradually increased. The levels in acute ischemia and reperfusion group were notably lower than sham group’s in 30～120 min. The levels in GM1 group were notably lower than sham group’s, and higher than acute ischemia and reperfusion group’s in 30～90 min(P<0.05).Conclusion After cerebral ischemia and reperfusion, GM1 can reduce lactate accymulation, and increase the amount of glucose, and enhance nerve cells’ survival rate, and provide obvious protective effects .
出处
《安徽医科大学学报》
CAS
2004年第6期449-452,共4页
Acta Universitatis Medicinalis Anhui
关键词
再灌注损伤
脑缺血
乳酸
葡萄糖
神经保护药
GM1
reperfusion injury
brain ischemia
lactic acid glucose
neuroprojective
agents
