中文摘要：

【目的】 探讨人工寒潮促发大鼠脑卒中发病前脑血管内皮细胞粘附分子（CAM）的变化;【方法】 110只SD大鼠制成双肾双夹肾血管性高血压大鼠模型,分为寒潮和非寒潮两大组,再按血压水平各分为正常血压组、160 - 199、200 - 219和 ≥ 220 mmHg等4个亚组,寒潮箱处理3 d后（每亚组6只大鼠）取视交叉平面脑片,连续切片,每8张取1张切片作免疫组化检测血管内皮的VCAM-1、ICAM-1、P-选择素水平,视交叉平面剩余切片及其余脑片连续切片,HE染色,了解是否有卒中病灶;发生脑卒中者被剔出统计学分析; 【结果】 在 〈 220 mmHg的各血压亚组,寒潮组各级脑血管的VCAM-1、ICAM-1、P-选择素的免疫组化阳性信号均比非寒潮组高;在 ≥ 220 mmHg血压亚组,寒潮组各级脑血管的上述指标的免疫组化阳性信号均比非寒潮组低;在非寒潮组,各级脑血管的三个指标的免疫组化阳性信号均随血压升高而升高;在寒潮组,各级脑血管的三个指标的免疫组化阳性信号也随血压升高而升高,然而在血压 ≥ 220 mmHg时转为降低; 【结论】 长期持续的高血压损害了脑血管内皮的调控功能,在寒潮等外因的诱导下易致脑卒中;

英文摘要：

[ Objective ] To investigate the changes of endothelial cellular adhesion molecules in brain vessels in rats with prestroke status caused by artificial cold. [Method] Male Sprague-Dawley （SD） rats （n = 110） were randomly assigned into 2 groups： artificial cold exposure （ACE） and non-ACE. Each group was further divided into 4 sub-groups according to their systolic blood pressure [after 2 kidney 2 clip renovascular hypertensive rats （RHR） operation]： （1） Sham-operated control group, BP 〈 140 mmHg, （2） mild hypertensive group, BP of 160- 199 mmHg, （3） moderate hypertensive group, BP of 200-219 mmHg, and （4） severe hypertensive group, BP t〉 220 mmHg. After ACE or non-ACE treatment, rat brains were removed quickly and then sectioned into 2.0-mm-thick coronal sections. One of every eight serial sections from bregma section were stained with immunohistochemistry for measurement of vascular cell adhesion molecule- 1 （VCAM- 1 ）, intercellular adhesion molecule- 1 （ICAM- 1 ）, and p-selectin. Other sections were stained with HE to observe whether stroke occurred. The rats with stroke did not enter the statistical analysis. [Result] （1） In Bp 〈 220 mmHg subgroup, all indexes were elevated in rats with ACE treatment compared with those with non-ACE treatment. On the other hand, all the indexes in Bp 〉t 220 mmHg subgroup decreased to some extent in rats with ACE treatment compared with those with non-ACE treatment. （2） Among the rats with not-ACE treatment, there is a positive association between high blood pressure and all indexes. Among rats with ACE treatment, this positive association can also be seen in the rats with Bp 〈 220 mmHg, however, all indexes decreased dramatically in rats with Bp ≥ 220 mmHg compared with those with Bp 〈 220 mmHg. [Conclusion ] Persistent and severe hypertension impairs the endothelial modulating function. Severe hypertensive RHR is prone to stroke after ACE.