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细胞间粘附分子-1和碱性成纤维细胞生长因子在脑梗死中的作用
引用本文:Song S,Zheng X,Wen S,Huang J,Ding D. 细胞间粘附分子-1和碱性成纤维细胞生长因子在脑梗死中的作用[J]. 中华医学杂志, 2002, 82(21): 1447-1449
作者姓名:Song S  Zheng X  Wen S  Huang J  Ding D
作者单位:1. 310009,杭州,浙江大学医学院附属第二医院神经内科
2. 杭州铁路医院内科
摘    要:目的了解脑梗死急性期血清可溶性细胞间粘附分子-1(sICAM-1)和碱性成纤维细胞生长因子(bFGF)的含量变化,以及在脑梗死发生发展过程中的作用.方法采用酶联免疫吸附法(ELISA) 检测55例急性期脑梗死患者和32例其他疾病对照组及30例正常健康人为对照组,测量血清sICAM-1和bFGF 含量.结果 (1)脑梗死患者血清sICAM-1和bFGF含量分别为766.2 μg/L±178.8 μg/L和17.4 μg/L±8.2 μg/L,较其他疾病对照组分别529.6 μg/±76.7 μg/L和8.3 μg/L±2.8 μg/L,正常健康对照组分别520.7 μg/±115.9 μg/L和5.8 μg/L±2.7 μg/L,差异有显著意义(P=0.000).(2)相关分析脑梗死时血清sICAM-1含量与bFGF含量呈正相关(r=0.471,P=0.000),与外周血白细胞数呈正相关(r=0.285,P=0.035),与神经功能缺损评分呈负相关(r=-0.333,P=0.013),而与血脂水平无明显相关关系(胆固醇r=-0.042,P=0.758;甘油三脂r=0.061,P=0.657).(3)脑梗死患者血清sICAM-1和bFGF含量与高血压史关系不密切.而bFGF含量与病灶大小有关.结论 ICAM-1和bFGF可能通过炎症机制参与了脑梗死的病理生理过程;急性期监测血清sICAM-1和bFGF含量变化有助于判断病情轻重和病灶大小.

关 键 词:脑梗死 细胞间粘附分子-1 碱性成纤维细胞生长因子
修稿时间:2002-06-20

Change of serum soluble intercellular adhesion molecule and basic fibroblast growth factor in patients with acute cerebral infarction and its clinical significance
Song Shuijiang,Zheng Xiaohong,Wen Shuqun,Huang Jianzheng,Ding Deyun. Change of serum soluble intercellular adhesion molecule and basic fibroblast growth factor in patients with acute cerebral infarction and its clinical significance[J]. Zhonghua yi xue za zhi, 2002, 82(21): 1447-1449
Authors:Song Shuijiang  Zheng Xiaohong  Wen Shuqun  Huang Jianzheng  Ding Deyun
Affiliation:Department of Neurology, The Second Affiliated Hospital, College of Medical Sciences, Zhejiang University, Hangzhou 310009, China.
Abstract:OBJECTIVE: To explore the changes of the levels of soluble intercellular adhesion molecule-1 (sICAM-1) and basic fibroblast growth factor (bFGF) in serum of patients with acute cerebral infarction, and the effects of sICAM-1 and bFGF on cerebral infarction. METHODS: ELISA was used to detect the serum sICAM-1 and bFGF of 55 patients with acute cerebral infarction (within 2 days) as well as 32 patients diagnosed as with other neurologic diseases (20 patients with sciatica and 12 with trigeminal neuralgia) and 30 healthy persons as controls. RESULTS: (1) Both serum sICAM-1 and bFGF in the infarction group were significantly higher [(766.2 +/- 178.8) micro g/L and (17.4 +/- 8.2) micro g/L respectively] than in other disease control group [(529.6 +/- 76.7) micro g/L and (8.3 +/- 2.8) micro g/L respectively] and normal control group [(520.7 +/- 115.9) micro g/L and (5.8 +/- 2.7) micro g/L respectively] (P = 0.000). (2) Correlation analysis showed that there was a positive correlation between the level of serum sICAM-1 and bFGF (r = 0.471, P = 0.000), the level of sICAM-1 was also positively correlated with the number of leukocytes at acute stage (r = 0.285, P = 0.035), and a negative correlation between sICAM-1 and European stroke scale (r = -0.333, P = 0.013) was found. No significant correlation was observed between the level of sICAM-1 and the levels of serum cholesterol (r = -0.042, P = 0.758) or triglyceride (r = 0.061, P = 0.675). (3) Blood pressure seemed to have no influence on the content of sICAM-1 and bFGF after cerebral infarction, while the level of serum bFGF with large infarct size was obviously higher at acute stage. CONCLUSION: The levels of sICAM-1 and bFGF increase significantly in the patients with acute cerebral infarction. sICAM-1 and bFGF mayin participate in the pathophysiologic process through inflammatory mechanism. The detection of serum sICAM-1 will be helpful in estimating the clinical severity and the determination of bFGF will be helpful in estimating the size of infarct lesion at acute stage of cerebral infarction.
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