To establish a model of coronary thrombotic microembolism in rats, either automicrothrombotic particulates (CM group) or saline control (SHAM group) was injected into temporarily clamped aortas of male Sprague-Dawley rats. After automicrothrombotic particulate injection, serum c-troponin I and von Willebrand factor levels, the no-flow area as evaluated by Thioflavin S, myocardial leukocyte infiltration levels, myocardial expressions of tumor necrosis factor ␣ and interleukin-6, the percentage of arterioles obstructed by thrombosis, and myocardial fibrosis were all significantly increased whereas cardiac function as evaluated by echocardiography and hemodynamic measurements were significantly reduced compared with the sham group. Thus, aortic automicrothrombotic particulate injection could induce coronary microembolism in rats, and this model could be of value in improving the understanding of pathophysiology of coronary microembolism. Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndrome and during coronary interventions.1 It does not always result in complete thrombotic occlusion of the epicardial coronary artery with subsequent impending myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation, which has recently been identified as a potential cause of no-reflow phenomenon, myocardium ischemia, and myocardial infarctlet. Atherosclerotic embolization in the microvasculature is associated with adverse prognosis. [1][2][3][4] Research results derived from suitable experimental models of coronary microembolism would help clinicians to understand the underlying pathological mechanisms and to develop effective therapies of coronary microembolism induced by atherosclerotic embolization in the microvasculature.5 Until now, plastic microspheres ranging from 20 to 900 m in diameter were injected into the coronary microcirculation to establish the coronary microembolism models in dog, swine and sheep.6 -11 Experimental models were also made by injecting adenosine-diphosphate or catecholamine to induce platelet aggregation in coronary microcirculation in pigs.12-13 However, injecting microspheres with unique sizing would only occlude respective vessels with comparable sizes, while thrombotic debris in patients might vary greatly in sizing and affect vessels with different diameters. Models using adenosine diphosphate or catecholamine could mimic the platelet aggregation process during coronary microthrombosis but could not reflect the influences of various embolism components of atherosclerotic plaques. Therefore, established coronary microembolism models could only partly mimic the in vivo situation of coronary microthrombosis. In the present study, we showed that coronary microembolism could be induced by intraaortic injection of automicrothrombotic particulates varying in sizing in rats. Increased myocardial inflammatory cells infiltration and fibrosis as well as reduced cardiac function w...