Objective:The present study was designed to test the hypothesis that inflam mation is involved in the end- or- gan damage(EOD) induced by sinoaortic denervation(SAD) in rats.Method:SAD was performed in male Sprague- Dawley rats at the age of1 0 weeks.U nder anaesthesia,aortic nerves were cut and the sinus region of the carotid artery was stripped and painted with1 0 % phenol.Pathological evaluation of EOD and the determ ination of plasm a or tissue levels of the factors relat- ed to inflam mation,including thromboxane B2 (TXB2 ) interleukin- 1 (IL- 1 ) ,tum our necrosis factorα(TNF- α) and reactive oxy- gen species(ROS) were perform ed at1 6 weeks after SAD.Pathological evaluation of EOD included heart weigh ratio,m yocar- dial and blood vessel hydroxyproline and collagen volume fraction,glomerular injury score and number of infiltrating inflam - matory cells.Indomethacin(2 0 mg/ kg per day,orally) or vitam in E(1 0 0 m g/ kg per day,orally) was administered for1 2 weeks,beginning from4 weeks after SAD,to observe their effects on SAD- induced EOD.Results:There were significantfibro- sis and inflamm atory infiltration in the myocardium and blood vessels,represented by higher hydroxyproline and collagen vol- ume fraction,and a large amount of inflamm atory cells in the tissues of SAD rats.Heart weight and kidney glomerular injury score were significantly higher in SAD than in sham operated rats.Plasma TBX2 ,TNF- α,IL- 1 and tissue ROS increased signifi- cantly after SAD.Indomethacin and vitamin E significantly decreased the contents of som e factors related to inflamm ation in SAD rats.Both drugs also alleviated m yocardial and vessel fibrosis,inflamm atory infiltration and kidney damage.Conclusion: Inflamm ation is involved in the organ dam age induced by SAD in rats Objective: The present study was designed to test the hypothesis that inflammations are involved in the end- or-gan damage (EOD) induced by sinoaortic denervation (SAD) in rats. Method: SAD was performed in male Sprague-Dawley rats at the age of 1 0 weeks. Uder an aesthesia, aortic nerves were cut and the sinus region of the carotid artery was stripped and painted with 10% phenol. Pathological evaluation of EOD and the determ ination of plasm a or tissue levels of the factors relat- ed to inflam mation, including thromboxane B2 (TXB2) interleukin-1 (IL-1), tum our necrosis factor α (TNF- α) and reactive oxy- gen species included heart weigh ratio, m yocar-dial and blood vessel hydroxyproline and collagen volume fraction, glomerular injury score and number of infiltrating inflammat - matory cells. Indomethacin (20 mg / kg per day, orally) or vitam in E (100 mg / kg per day, orally) was administered for1 2 weeks, begi nning from 4 weeks after SAD, to observe their effects on SAD-induced EOD. Results: There were significantfibro-sis and inflammtory infiltration in the myocardium and blood vessels, represented by higher hydroxyproline and collagen vol ume fraction, and a large amount of inflamm atory cells in the tissues of SAD rats. Heart weight and kidney glomerular injury score were significantly higher in SAD than in sham operated rats. Plasma TBX2, TNF- [alpha], IL-I and tissue ROS increased signifi- cantly after SAD. Indomethacin and vitamin E significantly decreased the contents of som e factors related to inflammtion in SAD rats. Both drugs also alleviated m yocardial and vessel fibrosis, inflammtory infiltration and kidney damage. Confusion: Inflammation is involved in the organ dam age induced by SAD in rats