摘要
目的研究血小板活化和血管内皮损伤标志物在脑卒中启动中的作用。方法300只SD大鼠分为模型组、假手术组和正常对照组,其中假手术组再分为假手术和假手术+内皮损伤组;模型组再分为高血压组、内皮损伤组和高血压+内皮损伤组;在第12周时使用寒潮箱处理各组大鼠,将各组大鼠再分为寒潮组和非寒潮组,其中寒潮组分别在寒潮前及寒潮后检测CD62p阳性表达率,免疫组织化学检测脑小血管细胞间黏附分子1的表达。结果模型组大鼠CD62p阳性表达率和细胞间黏附分子1的表达量高于正常对照组和假手术组(P<0.05);模型组大鼠经寒潮处理后CD62p阳性表达率和细胞间黏附分子1的表达量明显高于非寒潮组(P<0.05),其中高血压+内皮损伤组CD62p阳性表达率和细胞间黏附分子1的表达量更高(P<0.05)。结论长期的高血压损害了大鼠的内皮系统,而寒潮可以使这种损害加重,使其接近卒中前状态。
Aim To investigate the contribution of platelet activation and the damage marker of blood vessel endothelium in stroke.Methods 300 SD rats were divided into three groups： model group,sham operated group and normal control group,the sham operated group were divided into sham operated group and sham operated＋endothelium damage group;the model group were divided into hypertension group,endothelium damage group and hypertension＋endothelium damage group.In the 12th week the rats were divided into artificial cold exposure（ACE） and non-ACE,only ACE were endured by artificial climate cabinet,blood samples were collected for measuring CD62p expression and brain tissues were got to analyse intercellular adhesion molecule-1（ICAM-1） expression.Results In model group,the CD62p and ICAM-1 expression were higher than other groups（P0.05）;the CD62p and ICAM-1 expression in ACE（model group） were higher than non-ACE group（P0.05）;the CD62p and ICAM-1 expression in hypertension＋endothelium damage group was the highest in model group（P0.05）.Conclusion Persistent hypertension could damage the endothelium system of rat,artificial cold would worse this damage,and make it close to the state of pro-stroke.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2010年第2期114-116,共3页
Chinese Journal of Arteriosclerosis
基金
湖南省教育厅科学研究项目(06c708)
