Peskar B M, Lambrecht N, Stroff T, Respondek M, Müller K M
Department of Experimental Clinical Medicine, Ruhr-University of Bochum, Germany.
Dig Dis Sci. 1995 Nov;40(11):2460-4. doi: 10.1007/BF02063255.
Healing of ethanol-injured gastric mucosa was studied in rats treated with a neurotoxic dose of capsaicin to induce functional ablation of sensory nerves. Capsaicin treatment delayed the healing of mucosal damage in the glandular region and promoted the development of deep ulcerations predominantly in the antrum. These lesions occupied 86% of the antral surface and were associated with marked invasion of inflammatory cells and 18-fold elevation of gastric myeloperoxidase activity compared with vehicle-pretreated rats. Inhibition of cyclooxygenase, 5-lipoxygenase, or nitric oxide synthase did not affect the development of antral lesions after ethanol challenge in capsaicin-pretreated rats. In vehicle-pretreated rats, inhibition of nitric oxide synthase did not mimic the effect of functional ablation of sensory neurons. The findings suggest that in the gastric mucosa sensory neurons contribute to repair processes and limit the inflammatory response to injury. These effects do not involve arachidonic acid metabolites or nitric oxide.
