Restitution of barrier and transport function of porcine colon after acute mucosal injury.
Acute injury of the porcine colonic epithelium was induced in vivo with the bile salt, deoxycholate. A concentration of 15 mM for 30 min completely destroyed the surface epithelium and induced a marked increase in mucosal permeability to mannitol. The crypt epithelium however was not significantly affected. Within 8 min of recovery, the colonic surface was reepithelialized with flattened, migrating cells, and within 40 min, mucosal permeability to mannitol was normalized. In vitro studies showed that in these early stages of recovery, NaCl transport, short-circuit current, and resistance were markedly impaired, whereas the theophylline-induced secretory response remained intact. Recovery of absorptive function paralleled the transition from flattened to columnar surface epithelium and was complete within 2 h. Results suggest that 1) active migratory events play an important role in rapid restitution of an epithelial barrier, 2) active absorption of ions is much slower to recover, and 3) active secretory events are intact and probably originate in the crypt epithelium.
D000818:Animals; D001693:Biological Transport, Active; D002463:Cell Membrane Permeability / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism; D003106:Colon / Q000502:physiology*; D003840:Deoxycholic Acid; D004553:Electric Conductivity; D004848:Epithelium / Q000187:drug effects; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000502:physiology; D008353:Mannitol / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D013552:Swine; D013806:Theophylline / Q000494:pharmacology
D002712:Chlorides; D003840:Deoxycholic Acid; D008353:Mannitol; D012964:Sodium; D013806:Theophylline