Involvement of sensory afferent fibers and lipid peroxidation in the pathogenesis of stress-induced gastric mucosa damage.

Ablation of sensory nerves impairs healing of gastric ulcers, but the role of free radicals in the healing process has been little studied. The aim of our present investigations was to determine the participation of reactive oxygen species (ROS) in sensory nerve activity during WRS. Experiments were carried out on male Wistar rats and the number of gastric lesions was measured by planimetry. Colorimetric assays were used to determine gastric mucosal levels of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), as well as superoxide dismutase (SOD) activity. We found that capsaicin-inactivation of sensory nerves resulted in magnification of gastric mucosal damage induced by the WRS. In this process, oxidative stress occurs, as reflected by an increase of MDA and 4-HNE tissue concentrations (an index of lipid peroxidation), and a decrease of SOD activity, could play an important role. Pentoxyfilline-induced gastroprotection and hyperemia depends upon attenuation of the oxidative stress. This protection and hyperemia were, at least in part, attenuated by ASA. Afferent sensory fibers participate in the pathogenesis of ulcers. Lipid peroxidation plays an important role in this process.