Inflammation is involved in the organ damage induced by sinoaortic denervation in rats.
OBJECTIVE
The present study was designed to test the hypothesis that inflammation is involved in the end-organ damage (EOD) induced by sinoaortic denervation (SAD) in rats.


METHODS
SAD was performed in male Sprague-Dawley rats at the age of 10 weeks. Under anaesthesia, 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 determination of plasma or tissue levels of the factors related to inflammation, including thromboxane B2 (TXB2) interleukin-1 (IL-1), tumour necrosis factor alpha (TNF-alpha) and reactive oxygen species (ROS) were performed at 16 weeks after SAD. Pathological evaluation of EOD included heart weight ratio, myocardial and blood vessel hydroxyproline and collagen volume fraction, glomerular injury score and number of infiltrating inflammatory cells. Indomethacin (20 mg/kg per day, orally) or vitamin E (100 mg/kg per day, orally) was administered for 12 weeks, beginning from 4 weeks after SAD, to observe their effects on SAD-induced EOD.


RESULTS
There were significant fibrosis and inflammatory infiltration in the myocardium and blood vessels, represented by higher hydroxyproline and collagen volume fraction, and a large amount of inflammatory 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 TXB2, TNF-alpha, IL-1 and tissue ROS increased significantly after SAD. Indomethacin and vitamin E significantly decreased the contents of some factors related to inflammation in SAD rats. Both drugs also alleviated myocardial and vessel fibrosis, inflammatory infiltration and kidney damage.


CONCLUSIONS
Inflammation is involved in the organ damage induced by SAD in rats.
Department of Pharmacology, Second Military Medical University, Shanghai, China.
Chuan
C
Zhang
Hong
H
Chen
He-Hui
HH
Xie
He
H
Shu
Wen-Jun
WJ
Yuan
Ding-Feng
DF
Su
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D001011:Aorta / Q000378:metabolism; D001808:Blood Vessels / Q000378:metabolism; D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology; D003094:Collagen / Q000378:metabolism; D003714:Denervation; D005355:Fibrosis; D006909:Hydroxyproline / Q000378:metabolism; D007213:Indomethacin / Q000494:pharmacology; D018836:Inflammation Mediators / Q000097:blood*; D007375:Interleukin-1 / Q000097:blood; D007668:Kidney / Q000378:metabolism; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D012850:Sinus of Valsalva / Q000294:innervation*; D013929:Thromboxane B2 / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014810:Vitamin E / Q000494:pharmacology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D018836:Inflammation Mediators; D007375:Interleukin-1; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D014810:Vitamin E; D013929:Thromboxane B2; D003094:Collagen; D006909:Hydroxyproline; D007213:Indomethacin