摘要
目的观察尤瑞克林治疗急性脑梗死前后病人脑组织葡萄糖代谢、美国国立卫生院卒中量表(NIHSS)及改良残障水平评定量表(mRS)评分变化。方法44例脑梗死病人给予尤瑞克林0.15PNA单位,iv,gtt,qd,治疗7～14d,治疗前后对NIHSS和mRS评分进行比较。其中17例病人治疗前后进行脑PET-CT检查,观察病人脑葡萄糖代谢变化情况。结果NIHSS和mRS评分在治疗后均显著降低(均P=0.000)。17例病人经PET-CT检查,治疗前后对比,7例病灶缩小,病灶葡萄糖代谢率增高;3例病灶缩小,病灶葡萄糖代谢率无明显变化;2例病灶缩小,病灶葡萄糖代谢率稍降低;3例病灶大小无变化,病灶葡萄糖代谢率下降;2例病灶扩大或有新生病灶,病灶葡萄糖代谢率下降。结论尤瑞克林能够使急性脑梗死病人临床神经功能缺损明显好转,并能提高病人脑部葡萄糖代谢,改善预后。
AIM To observe the glucose metabolism in brain tissue and score changes of the National Institutes of Health Stroke Scale （NIHSS） and modified Rankin Scale （mRS） in patients with acute cerebral infarction （ACI） before and after treated with urinary kallidinogenase. METHODS Forty-four ACI patients were given urinary kallidinogenase 0.15 PNA U, iv, gtt, qd, for 7 - 14 days. The degrees of neurologic impairment of all the patients were observed and evaluated by NTHSS and mRS before and after the treatment, including 17 patients examined by positron emission tomography-computed tomography （PET-CT） before and after the treatment for observing the cerebral tissue glucose metabolism. RESULTS The nerve functional recovery occurred in all patients with statistical significances on NIHSS and mRS scores after the treatment （P = 0.000）. Seventeen patients examined with PET-CT showed seven of decrease in infarct sizes with increase of glucose metabolism; three with decrease of infarct sizes and no change in glucose metabolism; two with both decrease in infarct sizes and glucose metabolism; three with no change in infarct sizes but with decrease of glucose metabolism; and two with increase infarct sizes or newly formed infarct foci and decrease of glucose metabolism. CONCLUSION Urinary kallidinogenase provides significant improvement on the clinical nerve functional disorder with simultaneously promotion of cerebral glucose metabolism in patients with ACI.
出处
《中国新药与临床杂志》
CAS
CSCD
北大核心
2009年第9期709-712,共4页
Chinese Journal of New Drugs and Clinical Remedies
关键词
脑梗死
药物疗法
体层摄影术
发射型计算机
光瑞克林
cerebral infarction
drug therapy
tomography, emission-computed
urinary kallidinogenase
