Objective To establish an improved type Ⅱ cardio-renal syndrome rat model and evaluate it. Methods Twenty male SD rats were randomly divided into sham and model groups with 7 rats in the sham group and 13 rats in the model group. The model group received the method of squeezing the heart under a small animal anesthesia machine to permanently ligate the left anterior descending branch of the coronary artery to cause myocardial infarction. One week later, unilateral nephrectomy (right nephrectomy) was performed. The rats underwent cardiac echocardiography, pathological staining, and blood and urine tests at 6 weeks to verify model establishment. Results Compared with the sham group, the cardiac function assessed by echocardiography and the endogenous creatinine clearance rate in the model group rats were significantly decreased (P< 0. 01), and the levels of brain natriuretic peptide, blood creatinine, urea nitrogen, and 24 h urine protein in the model group were significantly increased (P< 0. 01). HE staining revealed a disordered myocardial arrangement, glomerular atrophy, and inflammatory cell infiltration in model group rats. Picric acid- Sirius red staining showed a significant increase in myocardial collagen fibers, an irregular arrangement of renal tubules, and a large amount of collagen deposition in model group rats. The positive staining area ratio was also significantly increased (P< 0. 01). Conclusions This improved modeling method provided a type Ⅱ cardio-renal syndrome rat model with s simple operation, minimal surgical trauma, and low mortality rate. This model simulates the early onset of cardiac and renal function damage and pathological changes in type Ⅱ CRS, laying the foundation for systematic and in-depth research on the pathogenesis and pathological mechanism of type Ⅱ cardio-renal syndrome.