BOLD-fMRI方法探讨尤瑞克林治疗急性脑梗死的疗效及其作用机制

目的 通过血氧水平依赖功能磁共振成像(BOLD-fMRI)的方法 观察尤瑞克林治疗急性脑梗死的疗效及其作用机制. 方法 将23例急性脑梗死患者按随机数字表法分成对照组(11例)和治疗组(12例),对照组给予常规治疗,治疗组在常规治疗的基础上加用尤瑞克林,疗程均为12～14d.观察治疗前后BOLD-fMRI影像和患侧手食指肌力评分和美国国立卫生研究院卒中量表(NIHSS)评分的变化. 结果 治疗后,治疗组息侧感觉运动皮层(SMC)激活频率和激活体积较治疗前明显增加(11/12 vs 4/12;199.58±169.41 vs 105.17±197.23),且治疗前后激活体积之差明显大于对照组(94.42±51.57 vs 16.09±106.61),差异有统计学意义(P<0.05);治疗后,治疗组患侧食指肌力评分和NIHSS评分较治疗前明显改善(2.67±1.44 vs 1.25±1.48;4.92±2.94 vs 10.42±3.80),且治疗前后NIHSS评分之差明显大于对照组(5.50±1.31 vs 3.18±2.48),差异有统计学意义(P<0.05). 结论 促进脑功能区SMC的激活恢复可能是尤瑞克林治疗脑梗死的一个重要机制.

Therapeutic effect of human urinary kallidinogenase in patients with acute cerebral infarction and its mechanism: evaluation by blood oxygen level dependent functional magnetic resonance imaging

Objective To investigate the therapeutic effect of human urinary kallidinogenase in patients with acute cerebral infarction and explore the mechanism by blood oxygen level dependent functional magnetic resonance imaging (BOLD-fMRI). Methods twenty-three patients with acute cerebral infarction were randomized into control group (n=11) and treatment group (n=12) to receive conventional treatment and additional human urinary kallidinogenase treatment for 12 to 14 days, respectively. BOLD-fMRI was performed, and the affected forefinger muscle strength and NIHSS score were recorded before and after the treatment. Results In the treatment group, the activated frequency and volume in the sensorimotor cortex (SMC) ipsilateral to the infarct increased significantly after the treatment (11/12 vs 4/12; 99.58±169.41 vs 105.17±197.23, P<0.05). The inerernent in the activated volume in the SMC was significantly greater in the treatment group than in the control group (94.42±51.57 vs 16.09±106.61, P<0.05). The forefinger muscle strength and NIHSS score in the treatment group improved significantly after treatment (2.67±1.44 vs 1.25±1.48; 4.92±2.94 vs 10.42±3.80, P<0.05), and the improvement in NIHSS score was significantly greater in the treatment group than in the control group (5.50±1.31 vs 3.18±2.48, P<0.05). Conclusion The therapeutic effect of human urinary kallidinogenase on acute cerebral infarction is mediated essentially by promoting the activation in the SMC in the functional area of the brain.