大鼠脑缺血再灌注血管壁NOS和ICAM-1的表达

EXPRESSION OF NOS AND ICAM-1 IN BRAIN VESSELS OF RATS WITH ISCHEMIA REPERFUSION INJURY

一氧化氮 (NO)和一氧化氮合酶 (NOS)与脑血管功能有重要关系 ,细胞间粘附分子 1 (ICAM- 1 )可由脑缺血/再灌注诱导产生并与脑组织损伤密切相关。本实验用免疫组织化学和 NADPH- d酶组织化学方法 ,观察了 SD大鼠实验性脑缺血再灌注内皮细胞 ICAM- 1和 NOS的表达。结果显示正常对照组大鼠脑血管 ICAM- 1免疫组织化学显色为阴性或弱阳性反应。再灌流 2 h,ICAM- 1阳性反应明显增强 ,与对照组相比 ,P<0 .0 1。随再灌流至 1 6 h,ICAM- 1表达增加近一倍。脑缺血 1 h缺血侧脑血管壁开始出现 NOS的阳性表达 ,与对照组相比 ,P<0 .0 1 ,再灌注 2 h,NOS表达最多 ,随后逐渐下降。结果提示脑缺血再灌注与 ICAM- 1和 NOS表达升高有关。

Nitric oxide (NO) and nitric oxide synthase (NOS) play an important role in cerebral ischemia. Intercellular adhesion molecule 1 (ICAM 1) can be induced by cerebral ischemia and reperfusion. The NOS and ICAM 1 expression in the vascular endothelial cells during ischemia and reperfusion in brains of SD rat was studied with histochemical and immunohistochemical methods. Results showed that ICAM 1 immunoreaction was negative or weak in normal control group. Compared with the control group it was significantly increased at 2h of reperfusion ( P <0 01) Up to 16h of reperfusion, the ICAM 1 expression nearly doubled. NOS staining was deep blue in color, appeared at 1h after ischemia. At 2h reperfusion, the NOS expression reached the peak, then decreased gradually. The results suggest that the increase of NOS and ICAM 1 expression in endothelial cells may be associated with cerebral ischemia and reperfusion in the rat.