K. J. Carter

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.

Effect of ethanol on frog gastric mucosa: Electrophysiologic and morphologic correlations

The effects of and recovery from luminal ethanol (0%-100%) were assessed in the in vitro chambered frog gastric mucosa. At concentrations of 5%-10%, the potential difference decreased during exposure, but recovered after washout. No gross or light microscopic changes were observed. During exposure to 20%-40% ethanol, potential difference and short circuit current decreased and resistance increased, with only partial recovery after removal of the alcohol. Acid secretion ceased at 20% ethanol and alkalinization of the luminal solution was observed at greater than or equal to 30% ethanol. Microscopy of this group showed discharge of mucus, separation of oxynticopeptic cells from the basal lamina, and slough of surface epithelium. At 60%-100% ethanol, potential difference and short circuit current decreased and resistance increased markedly but there was no recovery. Microscopy showed changes similar to those of the intermediate group (20%-40%), except that surface epithelial cells were fixed to the basal lamina rather than sloughing. The morphologic effects of 100% ethanol in vivo were similar to those in vitro. Pretreatment with 10(-5) M 16,16-dimethyl prostaglandin E2 did not prevent either the electrophysiologic or the histologic changes caused by 20% and 30% ethanol. We conclude that there is a gross discrepancy between the functional and morphologic findings after high concentrations of luminal ethanol.