Objective:To study the changes in coagulation function and inflammation levels during sepsis. Methods: Multiple infection sepsis model (MIM), based on cecal ligation and puncture (CLP), was apllied to establish a rat model of sepsis. Forty-eight male SD rats were randomly divided into blank group (control group, n=8), sham operation group (sham group, n=8), 4-hour sepsis group (4h group, n=8), 8-hour sepsis group (8h group, n=8), 12-hour sepsis group (12h group, n=8), and 16-hour sepsis group (16h group, n = 8). ELISA and coagulation analysis were used to detect inflammatory markers and coagulation-related indicators. Results: (1) Compared with the sham group, the content of LPS and IL-6 in the model rats of all time points increased significantly(p<0.001). The LPS and IL-6 gradually increased as the disease progressed, however no significant changes after 12 hours. (2) In the middle and late stages of the septic model(starting from the 8h), PT was significantly prolonged compared with that in the sham groups(p<0.01). (3) Compared with the sham group, APTT time was significantly prolonged in 8h,12h,and 16h groups(P<0.05,P<0.01). The APTT time gradually lengthened from 8h group, and gradually approached control group after that. (4) Except for 8h group, the Fbg content in septic groups of all time points increased significantly than sham group (p < 0.01). (5) There was a significant difference between control group and sham group in FDP (p < 0.01), but no significant difference between sham group and septic groups. (6) Compared with the sham group, the level of AT-III in each period of progression in sepsis was decrease(p < 0.01), and there were significant differences in the proportions of 4h group,8h group, and 16h group. Conclusion: In the progression of sepsis, infection and inflammation levels gradually increase and cause coagulation dysfunction. The Fbg increases rapidly in the disease progresses, indicating the rapid activation of ogenous after model surgery. However, the PT and APTT time significantly increase in the middle and late stages of sepsis, suggesting the coagulation factors gradually depleted to induce DIC. At the same periods, multiorgan damage caused by sepsis leads to reduced expression of AT-III, further aggravating the coagulation/anticoagulant disorders. In addition, during the disease progression, a large amount of FDP interferes with fibrin polymerization, resulting in hemorrhagetendency and worsening DIC.