中文摘要：

目的：探讨急性缺血缺氧早期小鼠脑组织的乳酸代谢过程,为采用9.4T高场磁共振频谱（9.4T1 H-MRS）测定乳酸水平的临床应用提供数据支持。方法：80只昆明小鼠按缺血缺氧造模时间随机分为16组,每组5只,每组小鼠急性脑缺血缺氧时间分别为0、20、40、60s和2、4、6、8、10、12、14、16、18、20min,以缺血缺氧0s组为对照组,采用9.4T1 H-MRS测定急性缺血缺氧早期小鼠脑乳酸水平。结果：在脑缺血缺氧20s时,小鼠脑组织中乳酸水平快速升高到峰值[（6.89±0.34）μmol·g^-1],缺血缺氧40s时开始缓慢下降,在缺血缺氧2min时下降最快,当缺血缺氧持续6min时乳酸水平下降到谷底并不再变化,形成平台期。与对照组比较,缺血缺氧不同时间组小鼠脑组织中乳酸水平均明显升高（P〈0.01）。结论：急性脑缺血缺氧40s可能是小鼠脑神经细胞无氧糖酵解的时间阈值,9.4T1 H-MRS可为测定脑组织乳酸代谢提供准确的时间窗。

英文摘要：

Objective：To explore the lactate metabolism in brain tissue of the mice with early acute hypoxiaischemia injury,and to provide data support for 9.4T1 H-NMR spectroscopy in detecting the lactate level clinically.Methods：Eighty Kunming mice were randomly divided into sixteen groups（0s,20 s,40s,60 s,2min,4min,6min,8 min,10 min,12 min,14 min,16 min,18 min,and 20 min）according to the duration of hypoxiaischemia（n=5）.The changes of lactate levels were detected by 9.4T1 H-NMR spectroscopy.Results：After the initiation of hypoxia-ischemia injury,the lactate level began to increase rapidly to the highest value of（6.89±0.34）μmol·g^-1 at 20 s,then started to decline quickly from 40 sto 2min,and eventually decreased to a stable level of（4.85±0.36）μmol·g^-1 until 6min.Compared with control group,the levels of lactate in brain tissue of the mice in hypoxic-ischemic groups were increased（P〈0.01）.Conclusion：40sof acute hypoxia-ischemia may be the lactate cerebral neuron threshold during the anaerobic glycolysis.9.4T1 H-MRS can provide the exact time window for detecting the lactate metabolism.