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.
Highlights
It has been verified that glycoprotein IIb/IIIa inhibitor tirofiban can attenuate myocardial no-reflow
It has been suggested that plugging of capillaries by leukocytes and platelet activation contribute to no-reflow [18, 19], these blood cell elements are not necessary for the development of this phenomenon, because no-reflow has been observed in buffer-perfused hearts as well [9, 20]
ET-1 is a peptide consisting of 21 amino acids, is one of three endothelins, and is the one produced by endothelium
Summary
Comparisons of data among all stages were performed with repeated-measures ANOVA followed by Student-NewmanKeuls test for multiple comparison. Comparisons of data among groups were done with one-way ANOVA followed by Student-Newman-Keuls test for multiple comparison. A value of P
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