infusion suggesting that, though the oesophageal mucosa might have been stimulated, the pain produced was not epigastric.We could not confirm that the cardiac sphincter pressure of those patients with epigastric pain was different from those without such pain.Moreover, radiological evidence of the capacity to herniate stomach, or of reflux of barium, as a measure of the incompetence of the anti-reflux mechanism, did not correspond with the incidence of epigastric pain.Hence we find little support for Earlam's hypothesis that the epigastric pain of duodenal ulcer is caused by acid stimulation of the oesophageal mucosa.
No takes yet. Share an insight, caveat, or question.
Smith et al. (1975) studied this question.
Synapse has enriched one closely related paper. Consider it for comparative context: