GASTRIC-MUCOSAL PROTECTION FROM ENTERAL NUTRIENTS - ROLE OF MOTILITY

Background: Cold restraint stress increases the force of gastric contr actions and produces gastric mucosal injury in rats. The aim of our st udy was to determine whether enteral glucose or hyperglycemia alone wo uld alter the stress-induced gastric motility pattern and ameliorate t he associated gastric mucosal injury. Methods: Adult male rats underwe nt surgical placement of gastric catheters, jugular venous catheters, and gastric strain gauge transducers 5 days before cold restraint. Thr ee groups of rats received different substances during the same cold r estraint stress protocol. Group 1 received 0.9% NaCl, 2 mL/h infused b oth intravenously (IV) and intragastrically (IG); group 2 received 0.9 % NaCl, 2 mL/h IG plus 25% glucose, 2 mL/h IV; and group 3 received 0. 9% NaCl, 2 mL/h IV plus 25% glucose IG. Following baseline gastric mot ility measurements, all rats were restrained for 2 hours at 20 degrees C followed by 2 hours at 4 degrees C. Results: Restraint even at room temperature increased the force of gastric contractions; the cold env ironment gradually prolonged gastric contractions. Enteral glucose blu nted the effects of stress on gastric motility, increased gastric resi dual volume, decreased gastric acidity, and prevented gastric mucosal injury. Parenteral glucose had little effect on any gastric parameters . Conclusions: Enteral glucose prevents the abnormal gastric motility pattern that is necessary to produce the gastric mucosal injury associ ated with cold restraint stress, but hyperglycemia alone has little ef fect on the pathophysiology of cold restraint. (C) 1998 by the America n College of Surgeons.