Colloidal bismuth subcitrate causes sustained release of gastric mucosal prostaglandin E2

Abstract

Gastric application of high doses of colloidal bismuth subcitrate (CBS) stimulates mucosal prostaglandin E2 (PGE2) production, which is considered part of the mechanism by which the drug accelerates peptic ulcer healing. Whether therapeutic, orally administered, doses of CBS cause a sustained stimulation of prostaglandin production is not known. We have, therefore, determined gastric luminal release of PGE2 during 'steady-state' perfusion of the stomach with CBS (10 mg/ml; isotonic mannitol 5 ml/min) and 4 h after the last oral dose of the drug (240 mg b.d.) for 2 weeks (isotonic mannitol 5 ml/min) in 8 healthy volunteers. A significant increase in PGE2 concentrations (712 (409-1076) vs. control 334 (252-655) pg/ml; medians with Q50 ranges; P less than 0.02) and PGE2 output (12.5 (7.3-14.3) vs. control 4.8 (4.1-7.3) ng/15 min; P less than 0.02) occurred during gastric perfusion with CBS. A similar increase in PGE2 concentrations (630 (297-1429) pg/ml; P less than 0.02) and PGE2 output (12.6 (6.4-22.2) ng/15 min; P less than 0.02) was observed following treatment with CBS for 2 weeks. These results suggest that therapeutic doses of CBS cause a sustained stimulation of gastric mucosal PGE2 formation.