GASTRODUODENAL MUCOSAL DEFENSE

The recognition that most peptic ulcer disease occurs as a consequence of either Helicobacter pylori infection or ingestion of nonsteroidal anti-inflammatory drugs has renewed interest in the hypothesis that ulcer disease occurs principally as a consequence of impaired mucosal defense. Studies published over the past year have advanced our understanding of the many complex interactions among the various components of mucosal defense, such as the microcirculatory response, mucus and bicarbonate secretion, and restitution. It is becoming increasingly clear that mediators such as nitric oxide, previously regarded solely as vasoactive substances, also affect the epithelium, parietal cells, and mast cells to produce effects that alter mucosal resistance to injury. Progress has also been made in understanding the influence of many mediators and growth factors on the ability of the mucosa to repair damage.