颞叶皮层梗塞大鼠磁共振T2加权像和氢磷谱的变化及蚓激酶的作用

摘要

目的：观察脑梗塞后组织水肿及物质能量 代谢的动态变化，以及蚓激酶的作用。rn方法：运用光化学法诱导的颞 叶皮层梗塞大鼠模型及磁共振成像和波谱技术。结果：梗塞组大鼠颞 叶皮层出现 一个体积和信号强度逐渐减小的T2高信号区；该区的NAA/(Cho+Cr)于梗塞后d1即有下降， 于d3和d5继续下降，且于d3，d5和d7与假手术组比较有显著性差异(P?.05)；该区的La c于梗塞后d1即有升高，于d5进一步升高，于d7仍处较高水平，而假手术组大鼠Lac一直 处于检测水平线以下。梗塞组大鼠全脑的βATP/(PME+PDE)，PCr/(PME+PDE)和βATP/PCr于 梗塞后d1即有下降，其后逐渐升高，且βATP/(PME+PDE)于梗塞后d1，d3和d5与假手术组比 较有显著性差异(P?.05)。蚓激酶能减小梗塞后d1高信号区的体积 (P?.05)，减 少梗塞后d7该区NAA/(Cho+Cr)的下降(P?.05)，减少梗塞后d1全脑βATP/(PME+PDE )的下降(P?.05)。结论：颞叶皮层梗塞后，梗塞灶出现组织水肿、神经元功能衰竭和数量减少，乳酸升高，全脑出现能量代谢障碍；而蚓激酶可使梗塞早期的组织 水肿减轻和全脑ATP增高，使梗塞后期的神经元功能受损减轻和神经元死亡减少。%Objective：To investigate the longitudinal changes of edema and substance and energy metabolism after cerebral infarction, rnand the e ffects of lumbrokinase.Methods：By means of the animal model of ph otochemically induced temporal cortical infarction and the technrnology of T2 we ighted magnetic resonance imaging (MRI),JH1，D，Z-and JP31，D，Z-magne tic resonance spectroscopy (MRS).Results：On the 1srnt,3rd,5th and 7 th day after i nfarction,a region of T2 hyperintensity was observed in left temporal neocorte x in infarction group and lumbrokirnnase group.The volume and T2 intensity of th e region gradually decreased from the 1st to the 7th day after infarction;the ra tio of NAA/(Cho+Cr) irnn the region in infarction group was significantly lower th an that in the corresponding region in sham-operated group on the 3rd,5th and 7 th day rnafter infarction respectively (P?.05); Lac appeared in the region in infarction group on the 1st,3rd,5th and 7th day after infarction, and warns not observed in the corresponding regio n in sham-operated group at all time points.Compared with sham-operated group, the ratio of βATP/(PMErn+PDE) of the whole brain in infarction group was signifi cantly lower on the 1st,3rd and 5th day after infarction respectively (P?.0 5). Lumbrornkinase significantly decreased the volume of the region of T2 hyperi ntensity on the 1st day after infarction (P?.05), significantly increasernd t he ratio of NAA/(Cho+Cr) of the region on the 7th day after infarction (P<0. 05), and significantly increased the ratio of βATP/(PME+PDE) of the wrnhole brain on the 1st day after infarction (P?.05).Conclusion：The resu lts indicated that the infracted region had severe edema, increased Lrnac and appa rent neuronal dysfunction and death,and energy metabolism of the whole brain de creased after focal infarction, and that lumbrokirnnase effectively ameliorated th e edema of infarcts and promoted energy metabolism of the whole brain at the ear ly stage of focal cerebral infarnrction, and decreased the neuronal dysfunction an d death in infarcts at the late stage.