Autonomic pathways in development of neural stimulation-induced gastric mucosal damage

Abstract

Gastric mucosal erosions can be induced by electrical stimulation of either vagus nerves (5 Hz, 5 V, 1 ms) or the paraventricular nucleus (PVN) of the hypothalamus (200 microA, 60 Hz, 100-microseconds pulse width). We have utilized various pharmacological and surgical interventions to determine the contributions of different components of the autonomic nervous system to the development of this neurally induced gastric damage in urethan-anesthetized Sprague-Dawley rats. In all experiments damage was assessed macroscopically and scored blindly on a 0 (normal) to 3 (severe) scale with samples sectioned for subsequent histological assessment of damage at the light microscopic level. Animals pretreated with either hexamethonium (30 mg/kg iv) or atropine (2 mg/kg iv) demonstrated reduced gastric damage scores after vagal stimulation compared with untreated control animals (P < 0.05). In contrast animals that underwent cervical cord transection exhibited gastric damage after both vagal and PVN stimulation that was not significantly different compared with animals with an intact cord undergoing similar stimulation (P > 0.05). Such cord transection itself did not cause any significant change to the gastric mucosa in the time period studied. These data emphasize the importance of the autonomic nervous system, in particular the parasympathetic component in the development of vagal stimulation-induced gastric damage. In addition, the present studies suggest that neither vagal nor PVN stimulation-induced gastric damage is dependent on neural projections to sympathetic preganglionic neurons of the intermediolateral cell column of the spinal cord.