No-reflow phenomenon due to cardiac microvascular dysfunction or disturbance aggravates clinic outcomes of a portion of patients with acute myocardial infarction undergoing percutaneous coronary intervention or thrombolytic therapy. Our working hypothesis was that cardiac microthrombosis would play an important role in the pathogenesis. We investigated that cardiac microthrombi were observed by Martius, Scarlet, Blue methocl (MSB) and Masson trichrome staining. Furthermore, we investigated the expression of fibrinogen-like protein 2 (fgl2) in rats with acute myocardial ischemia/reperfusion (MI/R) and its possible pathological and clinical significance. The fgl2 was highly expressed in myocardium of rats with acute MI/R and located at cardiac microvascular walls. We found that the expression of fgl2 in peripheral mononuclear cells of rats with acute MI/R significantly increased correspondingly with its cardiac expression. Expression of cardiac fgl2 was correlated with no-reflow size of rats with acute MI/R, which was detected and calculated by thioflavin S staining. No-reflow size was in line with cardiac diastolic dysfunction of rats with acute MI/R monitored by hemodynamics. Thus, microthrombosis is involved in cardiac microvascular dysfunction or disturbance of rats with acute MI/R as one cause, and fgl2 may emerge as a predictor of the occurrence of no-reflow phenomenon.