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
10.3760/cma.j.issn.1671-8925.2009.07.019
- VernacularTitle: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
- Author:
Fang YUAN
1
;
Tao HU
;
Yi-Dong WANG
;
Sui-Qiao HUANG
;
Jing-Rui PAN
;
Yu QIU
;
Ying PENG
Author Information
1. 中山大学附属第二医院
- Keywords:
Functional magnetic resonance imaging,blood oxygen level-dependent;
Cerebral infarction;
Kallikrein
- From:
Chinese Journal of Neuromedicine
2009;8(7):721-724
- CountryChina
- Language:Chinese
-
Abstract:
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.
