Abstract
It has been verified that glycoprotein IIb/IIIa inhibitor tirofiban can attenuate myocardial no-reflow. Myocardial no-reflow has been associated with alterations in endothelial junctions. In addition, ET-1 is an important mechanism for myocardial no-reflow. However, the effect of tirofiban on endothelial junctions and Endothelin-1 (ET-1) is unknown. Methods: Twenty-eight mini-swines were randomized into 3 study groups: 10 in control, 10 given an intravenous infusion of tirofiban and 8 in sham-operated. Acute myocardial infarction and reperfusion model was created with three-hour occlusion of the left anterior descending coronary artery followed by one-hour reperfusion. Results: In control group, plasma ET-1 significantly increased, ET-1 or VE-cadherin level in the reflow and no-reflow myocardium was significantly higher or lower than that in normal myocardium. Compared with the control group, tirofiban significantly decreased plasma ET-1 and myocardial tissue ET-1, maintained VE-cadherin level. Conclusions: Tirofiban is effective in preserving endothelial junction. This beneficial effect of tirofiban could be partly due to its reduction of ET-1.