Role of vagal hyperactivity in gastric stress ulceration after acute injury to the cervical cord

Abstract

The role of vagal hyperactivity in the pathogenesis of gastric stress ulceration that occurs after acute trauma to the cervical cord is controversial. We have used a rat model of transection of the cervical cord to induce gastric stress ulceration and to examine the cause of the ulcers. Cervical cord transection did not increase gastric acid output or plasma levels of gastrin or pancreatic polypeptide, either immediately or up to eight hours later. However, gastric stress ulceration showed a time-related increase in ulceration. Vagal stimulation with 2-deoxy-glucose enhanced the gastric acid output in rats with cervical cord transection but failed to change the quantity or characteristics of the gastric ulceration. We conclude that there is no evidence to support the vagal hyperactivity hypothesis in the pathogenesis of gastric stress ulceration after acute cervical cord injury.