Philip J. Goddard

Restitution of frog gastric mucosa in vitro: Effect of basic fibroblast growth factor

BACKGROUND Rapid re-epithelialization after superficial gastric mucosal injury is caused by migration of persisting viable epithelial cells. Basic fibroblast growth factor (bFGF) has been reported to enhance the healing of experimental duodenal ulcer, but its mode of action is unclear. The present experiments examine whether an effect of bFGF on restitution might contribute to such healing. METHODS Paired halves of bullfrog fundic gastric mucosa in Ussing chambers were injured by luminal exposure to 1 mol/L NaCl for 10 minutes. RESULTS Luminal protamine or suramin, both known to interfere with endogenous bFGF, significantly inhibited electrophysiological recovery at neutral luminal pH (pHL). Luminal sucrose octasulfate, which prevents acid degradation of bFGF, and an exogenous, acid-resistant form of bFGF allowed electrophysiological recovery at a pHL of 3.0 that completely prevented restitution in control tissues. Electrophysiological recovery correlated well with morphological restitution. The presence of endogenous bFGF in normal and restituting bullfrog mucosa was confirmed by positive staining with a monoclonal antibody. CONCLUSIONS It is concluded that rapid epithelial repair after surface injury is at least in part mediated by bFGF.

Present Views on Restitution of Gastrointestinal Epithelium

reviewed by Silen (15) and Lacy (16). A brief luminal exposure to hypertonic saline was used to induce superficial injury to oxyntic mucosa. Morphologically evident reepithelialization occurred concurrently with the return of mucosal electrophysiological parameters and the tissues ability to secrete acid. Restitution was found to take place in frog gastric mucosa over a 4-hr period (7) and somewhat more rapidly in the

In vitro recovery of canine gastric mucosal surface hydrophobicity and potential difference after aspirin damage.

This study determined how the luminal surface hydrophobicity and transmucosal potential difference (PD) of canine gastric mucosa changed during the recovery period after the tissue was challenged with acidified aspirin. Luminal aspirin reduced both the contact angle and PD of mucosae incubated in Ussing chambers. After the removal of aspirin, surface hydrophobicity was found to recover before PD, and nutrient 16,16-dimethyl prostaglandin E2 accelerated the recovery of both parameters. Restoration of luminal surface hydrophobicity may be an important component of how the stomach reestablishes its barrier properties after exposure to a luminal damaging agent.