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。
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.
出处
《吉林大学学报(医学版)》
CAS
CSCD
北大核心
2016年第4期690-693,共4页
Journal of Jilin University:Medicine Edition
基金
国家自然科学基金资助课题(30570480)
关键词
急性脑缺血
乳酸
脑代谢物
磁共振频谱
acute cerebral ischemia
lactate
cerebral metabolites
proton magnetic resonance spectroscopy