Role of Endothellial Cells in Reperfusion Injury : Studies on Mechanisms and Prohibition of Reperfusion Injury :

内皮细胞通过分泌EDRF、ET-1等调节血管张力，本实验研究了再灌注前后EDRF、ET-1的变化。本实验采用内皮细胞与血管平滑肌完全分离的模型，仅内皮细胞加入缺血再灌注损伤，应用Ca^++阻断剂研究其对内皮细胞的保护作用。当PMA活化的白细胞加入到缺血内皮细胞中时，EDRF的产生减少，ET-1的产生增加。在Ca^++阻断剂对内皮细胞的保护作用方面，细胞间Ca ^++阻断剂TMB-8和钌红在10 μ M/L浓度下对内皮细胞的保护作用最强。而细胞膜Ca^++阻滞剂尼卡地平则无保护作用。提示再灌注损伤是由于活化的白细胞粘附于内皮细胞，导致内皮细胞分泌EDRF减少，ET-1增加所致，对细胞间Ca^++升高的保护作用是重要的。

Endothelial cells control the vessel tension with the production of EDRF, endothelin-1(ET-1) and so on. We studied about changes of EDRF and ET-1 between before and after the reperfusion. We used Ca^<++>blockers for studying their protecting effects of endothelial cells from reperfusion injury.Our experimental model was perfectly separated endothelial cells and vessel smooth muscles, and only endothlial cells were added the ischemic and reperfusion damage. When activated leucocytes by PMA were added to ischemic edothelial cells, the production of EDRF decreased and the production of ET-1 increased. But when the attachments of endothelial cells and activated leucocytes were blocked by the filter, productions of EDRF and ET-1 had no change.As for protecting effects of endothelial cells by Ca^<++> blockers, TMB-8 and ruthenium red which are intercellular Ca^<++> blockers had the most protecting effect at the level of 10muM/L1. But nicardipine which is one of Ca^<++>blockers at the level of membrane had no protecting effect. It was concluded that reperfusion injury was caused when activated leucocytes attached endothelial cells and then the production of EDRF decrease and the production of ET-1 increased, and that it was important to protect the increase of intercellular Ca^<++>.