The effects of chemical sympathectomy and sensory nerve ablation on experimental colitis in the rat. McCafferty, Donna-Marie, John L. Wallace, and Keith A. Sharkey. Gastrointestinal and Neuroscience Research Groups, Faculty of Medicine, The University of Calgary, Calgary, Alberta, T2N 4N1, Canada
APStracts 3:0148G, 1996.
We assessed the effects of primary afferent nerve ablation (systemic treatment with capsaicin during the adult or neonatal periods), primary afferent nerve activation (intracolonic capsaicin), and sympathectomy (6-hydroxydopamine; 6-OHDA) on the development of colitis induced by trinitrobenzene sulfonic acid (TNBS) in rats. We also examined if lidocaine was effective after ablation of primary afferent nerves or sympathectomy. Colitis was assessed by macroscopic scoring, measurement of myeloperoxidase (MPO) activity and histology. Systemic capsaicin treatment in adults increased the macroscopic damage score. Capsaicin treatment of neonates did not significantly increase damage score or MPO activity compared to vehicle-treated controls. However, all capsaicin treated groups had a higher mortality. Intracolonic capsaicin treatment did not alter the severity of colitis. Chemical sympathectomy resulted in a decreased damage score and improved histology compared to controls. In 6-OHDA pretreated rats, lidocaine administration reduced the macroscopic and histological scores and MPO activity almost to control levels. However, lidocaine administration in capsaicin-treated rats attenuated the macroscopic damage but did not improve the MPO activity or histology. These data suggest that capsaicin-sensitive nerves play a protective role in experimental colitis and sympathetic nerves contribute to the development of colitis. The beneficial effects of lidocaine appears to be due primarily to its action on enteric nerves. 

Received 23 April 1996; accepted in final form 23 July 1996.
APS Manuscript Number G149-6.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 21 August 1996