摘要
目的研究急性脑梗死患者血清中神经元特异性烯醇化酶(NSE)、超敏C反应蛋白(hs-CRP)含量变化与神经功能缺损的关系及依达拉奉对急性脑梗死的影响。方法选择急性脑梗死患者90例,随机分为对照组(常规治疗)和依达拉奉组(依达拉奉+常规治疗,依达拉奉30 mg+0.9%氯化钠溶液100 mL,静脉滴注,2次/d,连续14 d),检测治疗前、治疗后7 d和14 d患者血清中NSE、hs-CRP和神经功能缺损的变化。结果急性脑梗死组患者血清神经元特异性烯醇酶、超敏C反应蛋白含量与神经功能缺损评分呈明显正相关(P<0.01)。治疗后,依达拉奉组患者血清NSE、hs-CRP水平降低,与对照组比较,差异均有统计学意义(P<0.05)。治疗后依达拉奉组的神经功能缺损评分明显低于对照组,两组比较差异有统计学意义(P<0.05)。结论急性脑梗死患者血清中NSE、hs-CRP含量升高,其含量可反映脑梗死的病情程度,可以作为脑梗死患者脑损害程度的客观指标。依达拉奉可以降低NSE和hs-CRP水平,能有效改善急性脑梗死的脑损害程度。
Objective To investigate the changes of serum neuron-specific enolase（NSE）,high-sensitivity Creactive protein（hs-CRP） levels and the relationship of NSE,hs-CRP levels w ith neurological function defect in acute cerebral infarction patients,and the influence of edaravone on it.Methods 90 patients w ith acute cerebral infarction w ere randomly divided into control group and edaravone group,the control group w ere given routine treatment,apart from routine therapy,the edaravone group w ere added edaravone 30 mg,tw ice a day,total of 14 d;the serum levels of NSE,hs-CRP and the change of neural function defect w ere investigated before treatment,7 d and 14 d after treatment.Results The serum levels of NSE,hs-CRP were in a positive correlation with the score of neurological function defect（P 0.01）.The edaravone group serum levels of NSE and hs-CRP were lower than those of control group（P 0.05） in invasion 7d after treatment.Score of NIHSS in the trial group w as low er than that of control group（P 0.05）.Conclusion The serum levels of NSE,hs-CRP increase in the patients with acute cerebral infraction,and they can reflect the degree of cerebral infraction,so they can be regarded as objective indexes judging the degree of brain damage.Edaravone can reduce the serum NSE and hs-CRP levels and promote the recovery of neurological function in patients w ith acute cerebral infarction.
出处
《实用药物与临床》
CAS
2011年第5期380-382,共3页
Practical Pharmacy and Clinical Remedies
关键词
急性脑梗死
神经元特异性烯醇化酶
超敏C反应蛋白
神经功能缺损
依达拉奉
Acute cerebral infarction
Neuron-specific enolase
High-sensitivity C-reactive protein
Neurological function defect
Edaravone
