首页> 中文期刊> 《磁共振成像》 >基于1H-MRS与LCModel软件检测健康青年人服用磷酸可待因后前额叶及海马代谢物变化

基于1H-MRS与LCModel软件检测健康青年人服用磷酸可待因后前额叶及海马代谢物变化

摘要

目的:通过绝对定量分析健康青年人服用磷酸可待因后双侧前额叶及海马代谢物浓度变化,为下一步研究青年人可待因慢性成瘾机制提供前期实验数据参考。材料与方法正常健康青年志愿者20名,男10名,女10名,年龄18~30岁,平均(24.9±1.9)岁,均为右利手,无神经、精神疾病病史。采用 GE 1.5 T Signa HDX超导MR扫描仪,单体素1H-MRS PRESS序列,TR 3000 ms, TE 30 ms,矩阵256×128,NEX为1,感兴趣区置于双侧前额叶及双侧海马,大小2 cm×2 cm×2 cm,采集服药前及口服60 mg磷酸可待因后1.0~2 h内的实验数据,利用LCModel软件对采集的数据进行后处理及定量,用SPSS19.0配对样本t检验进行统计学分析。结果服用磷酸可待因后左前额叶脑代谢物发生改变,甘油磷酸胆碱(GPC)浓度增加0.254 mmol/L、肌醇(Ins)浓度下降0.988 mmol/L,差异有统计学意义(n=13,P<0.05;n=12,P<0.05);右前额叶、双侧海马的代谢物浓度改变无统计学差异。结论口服磷酸可待因能引起左前额叶代谢物的改变,GPC浓度上升与Ins浓度下降可能与急性用药后前膜递质释放减少有关。%Objective: Absolute quantitative analysis of healthy youth in the bilateral prefrontal lobes and hippocampus were performed and offered preliminary stage experimental data, in order to supply a reference for the further study of codeine habituation.Materials and Methods: Twenty right-handed healthy youth were included [10 males, 10 females, mean age (24.9±1.9) years]. MRS data were collected by GE 1.5 T MR scanner, using point resolved selective spectroscopy (PRESS) sequence (TE/TR 30 ms/3000 ms). The regions of interest (ROI) were located over the bilateral prefrontal lobes and hippocampus, size of ROI was 2 cm × 2 cm × 2 cm. The data of spectra were post-processed by LCModel software and the concentrations of metabolites were ultimately measured. The metabolite concentration of each people was analyzed by paired-samples ttest of SPSS19.0.Results:After taking codeine phosphate, the concentration of GPC increased 0.254 mmol/L in the left prefrontal lobe while Ins declined 0.988 mmol/L, which reached statistical signiifcance (n=13,P<0.05. n=12,P<0.05). The alterations of metabolites in right prefrontal lobe and bilateral hippocampus did not reach statistical significance.Conclusions:The metabolites’ concentrations of the left prefrontal lobes would change with oral codeine phosphate. GPC increased in the left prefrontal lobe while Ins declined, which was considered related with the abatement of neurotransmitter.

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