The focus was on salivary glands in
cysteamine-induced
duodenal ulcer and the different effects of antiulcer agents on
cysteamine-induced
duodenal ulcer in sialoadenectomized but not gastrectomized rats. We tested antiulcer agents on
cysteamine-induced
duodenal ulcer in rats (agents/kg i.p.) simultaneously with
cysteamine 400 mg/kg s.c., rat killed 24 h thereafter subjected to no surgery (normal), to
gastrectomy (24 h before) or sialoadenectomy, acute (24 h before) or chronic (21 days before). (i) Ulcerogenesis:
cysteamine-induced
duodenal ulcer had the same severity and incidence in normal, gastrectomized or acutely or chronically sialoadenectomized rats. (ii) Antiulcer effect under normal conditions or following
gastrectomy: in normal or gastrectomized rats all agents tested, gastric pentadecapeptide
BPC 157 [currently in clinical trials for
inflammatory bowel disease (PL-10, PLD-116, PL-14736, Pliva) (10.0 microg or 10.0 ng),
ranitidine (10 mg),
atropine (10 mg),
omeprazole (10 mg)] inhibited
cysteamine-induced
duodenal ulcers, acting through gastric acid-independent mechanisms. Following sialoadenectomy, acute or chronic:
ranitidine,
omeprazole and
atropine were completely ineffective, while pentadecapeptide
BPC 157 could protect. Thus, we found that contrary to stomach, salivary glands are implicated in cytoprotective agent activity (standard agents were ineffective after sialoadenectomy). Also, gastric pentadecapeptide
BPC 157 was consistently associated with a cytoprotective effect, suggesting a beneficial activity distinctive from that of H2-receptor blockers,
proton-pump inhibitors and
anticholinergics; but probably replacing missing salivary glands factors.