论文部分内容阅读
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。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 <0 .0 5 ) ;该区的Lac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 <0 .0 5 )。蚓激酶能减小梗塞后d1高信号区的体积 (P <0 .0 5 ) ,减少梗塞后d7该区NAA/ (Cho +Cr)的下降 (P <0 .0 5 ) ,减少梗塞后d1全脑 βATP/ (PME +PDE)的下降 (P <0 .0 5 )。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 observe the dynamic changes of tissue edema and substance energy metabolism after cerebral infarction, and the effect of lumbrokinase. Methods: The rat models of temporal lobe cortex infarction induced by photochemical method and magnetic resonance imaging and spectroscopic techniques were used. Results: In the infarct group, there was a T2 high signal region in the temporal cortex with a gradually decreasing signal intensity. The NAA / (Cho + Cr) in this region decreased at d1 after infarction and continued to decrease at d3 and d5 There was a significant difference between d3, d5 and d7 in the sham operation group (P <0.05). The Lac in this area increased at d1 after infarction and further increased at d5, and remained high at d7 , Whereas sham-operated rat Lac was always below the detection level. The levels of βATP / (PME + PDE), PCr / (PME + PDE) and βATP / PCr in whole brain of infarcted rats decreased after d1 and then gradually increased, and the ratio of βATP / (PME + PDE) After d1, d3 and d5 compared with the sham group had significant differences (P <0. 05). Lumbrokinase could decrease the volume of d1 high signal area after infarction (P <0.05), reduce the decrease of NAA / (Cho + Cr) in d7 area after infarction (P <0.05), reduce the d1 Whole brain βATP / (PME + PDE) decreased (P <0.05). Conclusion: After infarction of temporal cortex, tissue edema, neuron failure and quantity decrease, lactic acid increase and whole brain appear energy metabolism disorder. However, lumbrokinase can reduce edema in early infarction and increase whole brain ATP, So that late neurological impairment of infarction and reduce neuronal death.