Rapid repair of injured gastric mucosa.
The morphology of the rat gastric mucosa superficially damaged by a 30-45 sec exposure to 100% ethanol caused over 99% of the luminal surface to be necrotic without extensive hemorrhage or hyperemia. However, this damaged area restituted or rapidly healed and the process was described. These findings were compared with in vitro gastric mucosae of bullfrogs and guinea pigs which were damaged with 1 or 1.25 M NaCl and allowed to restitute. The rat gastric mucosa showed evidence of cell migration within 5 min after ethanol damage and after 15 min as much as 50% of the denuded basement membrane was restituted. After 30 min about 75% of the mucosa was covered with cells and by 1 h there were only minor epithelial discontinuities. The in vitro frog mucosal restitution after hypertonic injury was slower and required 1-2 h to show appreciable cell migration and 4-6 h for completion of the repair process. Using chambered guinea pig gastric mucosa damaged with hypertonic NaCl restituted the necrotic surface almost as rapidly as the intact rat stomach necrotized with absolute ethanol. Since prostaglandin treatment did not prevent ethanol or hypertonic salt injury or affect the restitution process it was proposed that the term cytoprotection as it is generally used is not appropriate.
D000818:Animals; D002470:Cell Survival; D004594:Electrophysiology; D004848:Epithelium / Q000473:pathology / Q000502:physiology; D000431:Ethanol / Q000633:toxicity; D005753:Gastric Mucosa / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D006168:Guinea Pigs; D009336:Necrosis; D011892:Rana catesbeiana; D051381:Rats; D014945:Wound Healing
D000431:Ethanol