脑梗塞患者血浆ADMA水平与脑血管反应性的相关性研究
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摘要
目的
     本实验通过测定脑梗塞患者血浆ADMA水平、脑血管反应性,研究血浆ADMA水平、脑血管反应性与脑梗塞的关系及血浆ADMA与脑血管反应性的相关性,以探讨ADMA在脑血管调节中的作用。
     方法
     选择2009年2月至2010年1月在苏州大学附属第一医院神经内科住院的急性脑梗塞患者57例为病例组,其中动脉粥样硬化性脑梗塞(AI)30例,腔隙性脑梗塞(LI)27例;另选取年龄及性别构成与病例组相匹配的在我院体检者25例为对照组,用酶联免疫吸附法(ELISA)测定其血浆ADMA,全自动生化分析仪测定其空腹血糖、甘油三酯、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇等生化指标,同时通过颈动脉超声检测颈动脉内膜-中膜厚度(IMT),经颅多普勒超声检测脑血流动力学变化,并记录相关参数值,计算屏气指数,应用SPSS16.0软件进行统计分析。
     结果
     1、动脉粥样硬化性脑梗塞及腔隙性脑梗塞组BHI水平显著低于正常对照组(P<0.05);组间差别无统计学意义(P>0.05)。
     2、动脉粥样硬化性脑梗塞及腔隙性脑梗塞组血浆ADMA水平高于正常对照组(P<0.05),且动脉粥样硬化性脑梗塞组血浆ADMA水平高于腔隙性脑梗塞组(P<0.05)。
     3、Logistic回归分析显示:收缩压、颈动脉内-中膜厚度、BHI、ADMA为脑梗塞的独立危险因素。
     4、BHI与高密度脂蛋白呈正相关,与颈动脉内-中膜厚度呈负相关。
     5、ADMA与收缩压、颈动脉内-中膜厚度、甘油三脂、总胆固醇呈正相关。
     6、偏相关分析显示BHI与ADMA呈负相关。
     结论
     1、急性脑梗塞患者血浆ADMA水平升高、脑血管反应性降低,血浆ADMA、脑血管反应性可能为脑梗塞的独立危险因素。
     2、血浆ADMA水平与脑血管反应性呈负相关,与收缩压、颈动脉内-中膜厚度、甘油三脂、总胆固醇呈正相关。ADMA水平升高可影响血管内皮功能,降低脑血管反应性,从而促进脑梗塞的发生发展。
Objective
     This study observed the relationship among ADMA,cerebrovascular reactivity and cerebral infarction, and the correlation between ADMA and cerebrovascular reactivity through measuring the level of plasma asymmetric dimethylarginine (ADMA) , cerebrovascular reactivity of cerebral infarction patients, to explore the role of ADMA in cerebrovascular autoregulation .
     Methods
     The study was designed in the first hospital affiliated to Soochow University between February 2009 and January 2010. we selected Fifty-seven patients with cerebral infarction .atherothrombotic infarction (AI)group ( n=30 ), lacunar infarction(LI) group(n=27),and 25sex-and age-matched healthy volunteers. plasma asymmetric dimethylarginine were measured by enzyme linked immunosorbent assay (ELISA), whereas fasting plasma glucose, triglycerides, total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol were measured by automatic biochemistry analyzer. and in the same time carotid artery intima-media thickness were examined by using neck artery ultrasound.Cerebral hemodynamics changes were measured by transcranial Doppler.and recorded the hemorheological parameters,and calculated the breath-holding index . All statistical analysis were performed using the Statistical Package for Social Science(SPSS for Windows, Version 16.0)
     Results
     1 The breath-holding index of atherothrombotic infarction group and lacunar infarction group were significantly lower than normal contro(lP<0.05). but the difference of sub-group was not significant (P>0.05).
     2 Plasma asymmetric dimethylarginine levels of atherothrombotic infarction group and lacunar infarction group were significantly higher than normal control(P<0.05).and plasma asymmetric dimethylarginine levels of atherothrombotic infarction group was significantly higher than lacunar infarction group(P<0.05).
     3 Logistic regression analysis showed that systolic pressure. carotid artery intima-media thickness the breath-holding index and ADMA were respectively independent risk factor for cerebral infarction.
     4 The breath-holding index was positively correlated with high density lipoprotein cholesterol,and was negatively correlated with carotid artery intima-media thickness.
     5 Asymmetric dimethylarginine were positively correlated with systolic pressure. carotid artery intima-media thickness. triglyceride.total cholesterol.
     6 The partial correlation analysis suggested that the breath-holding index was negatively correlated with ADMA .
     Conclusions
     1 The plasma asymmetric dimethylarginine levels of acute cerebral infarction patients was increased, cerebrovascular reactivity was decreased, plasma ADMA, cerebrovascular reactivity may be independent risk factors of cerebral infarction.
     2 Plasma asymmetric dimethylarginine levels was negatively correlated with cerebrovascular reactivity, positively correlated with systolic pressure. carotid artery intima-media thickness. triglyceride.total cholesterol .the elevated plasma asymmetric dimethylarginine levels may affected endothelial function,reduced the cerebrovascular reactivity, then promoting the development of cerebral infarction.
引文
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