Objective The purpose of this study was to explore a method of coronary heart disease model of qi- deficiency and blood-stasis syndrome type in rats by comparing the tongue appearance and its relationship with prostacyclin (PGI₂) and thromboxane A2 (TXA₂) of three different model estalishment method ,which were respectively established by pathological factors, etiological factors and compoundfactors. Methods Thirty-two rats were randomly divided into four groups: Group K:Normal food and water ( n = 8); Group L: normal feeding twenty-one days and then ligation the left anterior descending coronary artery (n = 8); Group Y:control diet combine with exhautive swimming for twenty-one days (n = 8); Group F: control diet combine with exhautive swimming for twenty-one daysand then ligation the left anterior descending coronary artery ( n = 8). At the end of modeling, Photoshop 6. 0 was used to analyze the RGB value of the tongue surface and an RGB data distribution range table was used to evaluate the tongue color of each model. HE staining was used to determine the numbers of microvessels in the upper cortex, keratinized layer, lamina propria, and lamina propria. Immunohistochemistry was used to analyze the positive expression rate of PGI₂ and TXA₂, and calculate the T/ P ratio. Results (1) The tongue quality in Group K was in the category of “light red tongue”. In Group L, the R value of the tongue surface was significantly lower than that in Group K, reflecting “dark red tongue”. In Group Y, the R value of the tongue surface was also significantly lower than that in Group K, reflecting “ light white tongue”. In Group F, the R value, G value, and B value of the tongue surface were significantly lower than those in Groups K and L, reflecting “purple tongue”. (2) Compared with Group K, there were no differences in the height of each layer and the number of microvessels of the filiform papilla on the lingual surface in Group L. Compared with Group K, there was a significant decrease in the height of the keratosis layer of filiform papilla in Group Y. In Group F, there were significant differences in the height and number of microvessels between Group K and Group L, while there was no difference in the height of the lamina propria in each group. (3) Compared with that in Group K, there were no significant changes of PGI₂ in Groups L, Y, and F. The TXA₂ level and the ratio of T/ P in Group L were significantly higher than those in Group K. The TXA₂ level and the ratio of T/ P in Group F were significantly higher than those in Group K and Group L. Conclusions The RGB quantitative characteristics of tongue color of CHD with qi deficiency and blood stasis syndrome are related to the decrease of the height of the suprapapillary cortex and keratodermis, and the increase of the number of capillaries in the lamina propria. The molecular biological mechanism may be related to the imbalance of TXA₂ / PGI₂ . The pathological etiology complex model is more consistent with the characteristics of CHD with qi deficiency and blood stasis syndrome.