Objective: To establish and evaluate the old rat model with Ganqi stagnation syndromes of insomnia. Method: Wistar rats were randomly divided into 4 groups:control

single-factor model

the multi-factor model

the multi-factor model+Shuyu Anshen Fang treatment. The old rat model with Ganqi stagnation Syndromes of insomnia was induced by intraperitoneal injection of D-galactose 60 mg· kg-1·d-1 for six weeks

and then clamping tail stimulus for one week was used toestablish Ganqi stagnation model

and REM sleep deprivation for 48 hours was caried out by using modified multiple platform method (MMPM). Then features of physical sign

free radicals in brain

and the contents of 6-keto-prostaglandin F1a(6-keto-PGF1a)

thromboxane B2(TXB2) in blood plasma were analyzed. Result: Compared with all the other groups (control group

treatment group and single-factor model group)

the multi-factor model group with Ganqi stagnation showed the higher levels of malondialdehyde(MDA) and TXB2(P<0.01)

and the lower levels of superoxide dismutase (SOD)

6-keto-PGF1a and the ratio of 6-keto-PGF1a/TXB2 (P<0.01). Conclusion: The composite animal model showed pathological features of clinical Ganqi stagnation syndromes. It is a feasible and reliable composite animal model.