AUTONOMIC PATHWAYS IN DEVELOPMENT OF NEURAL STIMULATION-INDUCED GASTRIC-MUCOSAL DAMAGE

Gastric mucosal erosions can be induced by electrical stimulation of e ither vagus nerves (5 Hz, 5 V, 1 ms) or the paraventricular nucleus (P VN) of the hypothalamus (200 mu A, 60 Hz, 100-mu s pulse width). We ha ve utilized various pharmacological and surgical interventions to dete rmine the contributions of different components of the autonomic nervo us system to the development of this neurally induced gastric damage i n 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 asses sment of damage at the light microscopic level. Animals pretreated wit h either hexamethonium (30 mg/kg iv) or atropine (2 mg/kg iv) demonstr ated reduced gastric damage scores after vagal stimulation compared wi th untreated control animals (P < 0.05). In contrast animals that unde rwent cervical cord transection exhibited gastric damage after both va gal 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 chang e to the gastric mucosa in the time period studied. These data emphasi ze the importance of the autonomic nervous system, in particular the p arasympathetic component in the development of vagal stimulation-induc ed gastric damage. In addition, the present studies suggest that neith er vagal nor PVN stimulation-induced gastric damage is dependent on ne ural projections to sympathetic preganglionic neurons of the intermedi olateral cell column of the spinal cord.