Esophagitis results from excessive exposure of the esophagus to gastric jui
ce through art ineffective or dysfunctional lo,ver esophageal sphincter mec
hanism. A possible role of pepsin in damaging the esophageal mucosa with co
nsequent esophagitis may be examined directly by testing pepsin under vario
us conditions in experimental models of esophagitis. Since gastric juice co
ntains both acid and pepsin, all experiments examine separately effects of
perfusion of the esophagus by acid without and with pepsin in various combi
nations. Acid perfusion alone at concentrations represented by pH 1.3 or ab
ove does not produce esophagitis. The addition of pepsin to acid between pH
1 and 3.5 causes considerable acute esophageal damage. Outside the proteol
ytic range, i.e., higher than pH 3.5, pepsin does not damage the esophagus.
The damage caused by acidified pepsin may be made much worse by the furthe
r addition of aspirin or other NSAIDs, presumably by further breaking down
mucosal barriers.