摘要
目的:探讨缺血再灌注时大鼠视网膜组织型纤溶酶原激活物(tissue-type plasminOgen activator,TPA)活性与视网膜微血管外基质降解的相关性。方法:采用眼压升降法造成视网膜缺血后再灌注。实验组分缺血1-2 h再灌注1-2 h各组。各组视网膜测试TPA的活性,并用免疫组化法对视网膜微血管外基质作Ⅳ型胶原、层粘连蛋白和纤维粘连蛋白染色。结果:缺血再灌注后,大鼠视网膜TPA的活性随缺血和再灌注时间的延长而显著升高;实验组的Ⅳ型胶原、层粘连蛋白和纤维粘连蛋白阳性染色平均单位面积显著地小于正常对照组,阳性染色呈不连续线状的微血管数显著地多于正常对照组。结论:缺血再灌注可引起视网膜TPA的活性升高,使微血管外基质降解,破坏血-视网膜屏障,导致视网膜结构和功能损伤。
To explore the correlation between the activity of tissue-type plasminogen activator （TPA） and extracellular matrix （ECM） around microvessel in retina of rats during ischemia and reperfusion. Methods： The models of retinal ischemia-reperfusion were made by raising and lowering the intraocular pressure （IOP）. The experimental groups were divided into ischemia 1-2 hours and reperfusion 1-2 hours groups. The activity of TPA in the retina of each group was measured, and the type Ⅳ collagen, larninin and fibronectin around retinal microvessel were stained by the immunohistochemistry. Results： During ischemia and reperfusion, the activity of TPA in the retina of rats increased markedly following the prolongation of ischemia-reperfusion. Average areas of positive reaction of the type Ⅳ collagen, laminin and fibronectin around retinal microvessel during ischemia and reperfusion were less than that of normal retina. The microvessel counts of discontinuous positive reaction of the type Ⅳ collagen, laminin and fibronectin around retinal microvessel during ischemia and reperfusion were more than that of normal retina. Conclusion： Ischemia and reperfusion can raise the activity of TPA in the retina of rats, which may degrade the extracellular matrix around the retinal microvessel, destroy the barrier of blood-retina and damage the retinal structure and function.
出处
《解剖学杂志》
CAS
CSCD
北大核心
2005年第4期405-407,i0001,共4页
Chinese Journal of Anatomy
