The Role of Motility in Gastric Mucosal Injury and Protection

Abstract

Several animal studies have helped to investigate the role of motility in gastric mucosal injury. The administration of solid food to rats receiving subcutaneous indomethacin (indometacin) 30 mgj kg reduced the incidence of lesions in the body of the stomach compared with that in rats receiving indomethacin alone; however, lesions in the antrum and intestine became more prominent, and it was proposed that increased antral activity was involved in this mechanism. Similarly, fasted rats who received indomethacin and then were fed developed antral ulcers. However, a low residue diet decreased the incidence and number of lesions, although it is not known whether such a diet affects gastric motility. To determine whether stomach lesions, induced by cold-restraint stress in rats, were a result of increased acid secretion or increased gastric motility, animals were given papaverine, a strong smooth muscle inhibitor. The antral lesions decreased and it was postulated that, at least in this model, antral ulcers were mainly a result . of increased gastric antral motility, with antral contractions in these animals being more prolonged and of higher amplitude. Although it is difficult to extrapolate these results to the human situation, information suggests that gastric emptying is accelerated in duodenal ulcer patients, presumably resulting in increased acid delivery to the duodenal bulb. Studies in animals with induced duodenal ulcers indicated that increased duodenal motility was associated with an increased clearance of bicarbonate, reducing the buffering capacity in the duodenal bulb. However, measurement of duodenal transit and duodenal bulb clearance in patients with active or inactive duodenal ulcer failed to demonstrate any differences from a control group, suggesting this may not be a mechanism in humans. In patients with gastric ulcers, antral contractions are decreased and this may be related to impaired or delayed gastric emptying. Additionally, decreased pyloric pressure has been demonstrated and there is some evidence for increased duodenalgastric reflux in these patients. However, it has not been demonstrated that increased duodenalgastric reflux produces gastritis or gastric ulcer, and, after gastric ulcer healing, abnormal antral motility, decreased pyloric pressure and increased duodenal-gastric reflux persist. Thus, the role of . duodenal-gastric reflux in the pathogenesis of gastric lesions, particularly of gastric ulcer, remains questionable. In animal studies, stress has been associated with a decrease in antral contractions. However, in general, the response depends on the type of stress used, and both humans and animals may adapt to repeated stress by producing a change in response. In conclusion, the role of motility in gastric mucosal injury and protection remains to be defined, and as yet there is no strong evidence that motility per se is an important predisposing factor in gastroduodenal mucosal lesions.