心肌缺血再灌注后可引起心肌的凋亡、自噬及心脏功能障碍，我们研究发现，心肌缺血再灌注后外周血微粒明显增加，这些微粒通过影响钙瞬变而引起心脏收缩功能障碍，但具体机制尚不明确。我们以前研究发现，细胞受损后释放的内源性危险信号可通过激活TLRs/IκB/NF-κB途径，促进心肌细胞产生ILs、TNF-α等细胞因子，TNF-α可抑制心肌细胞对Ca2+再摄取。因此我们认为心肌缺血再灌注损伤后，外周血微粒可能作为内源性危险信号，刺激细胞产生细胞因子，引起心肌收缩功能障碍。本实验拟急性心肌梗死患者、小鼠和心肌细胞为研究对象，通过多种实验技术从细胞、组织、器官及整体水平来探讨心肌缺血再灌注损伤释放的微粒引起心脏收缩功能障碍的机制，这将初步明确微粒促进I/R损伤心脏收缩功能障碍的作用机制，为临床上心肌保护提供新策略。

Myocardial ischemia/ reperfusion (MI/R) can cause myocardial apoptosis, autophagy and cardiac dysfunction. We have found that peripheral blood particles are increasing significantly after MI/R. These particles cause cardiac systolic dysfunction by affecting calcium transients. However, the specific mechanism is not clear. Our previous studies have found that endogenous risk signals released after cell damage can promote cardiomyocytes to produce ILs, TNF-α and other cytokines by activating TLRs/IκB/NF-κB pathway, and TNF-α can inhibit cardiomyocytes against Ca2+ re-uptake. Therefore, we believe that peripheral blood microparticles may act as endogenous risk signals after MI/R injury, stimulating cells to produce cytokines, causing myocardial contractile dysfunction. This study intends to use acute myocardial infarction patients, mice and cardiomyocytes as research objects, through a variety of experimental techniques to explore the release of granules from MI/R injury from cells, tissues, organs and overall levels. The mechanism of dysfunction, which will preliminarily define the mechanism of action of microparticles to promote I/R injury to cardiac systolic dysfunction, meanwhile provide a new strategy for clinical myocardial protection.