title: Mucosal permeability changes during intestinal reperfusion injury. The role of mast cells.
abstract: The objective of this study was to investigate the role of intestinal mast cells in mucosal functional and morphological alterations induced by 30 min segmental ischemia and 120 min reperfusion in anesthetized dogs. The time course of permeability changes of the mucosa to sodium fluorescein (NaFl) in blood-lumen and lumen-blood directions was studied in two separate series of experiments. Local hemodynamics, intramucosal pH (pHi) alterations, mast cell number and degranulation and the degree of tissue injury were determined. The effects of cromolyn (peritoneal-type mast cell stabilizer), quercetin (mucosal-type mast cell stabilizer), and dexamethasone (aspecific membrane stabilizer and mast cell depleter) pretreatments were evaluated. Ischemia-reperfusion induced significant tissue injury, elevated segmental vascular resistance, and decreased pHi. The blood to lumen clearance of NaFl increased significantly during ischemia and reperfusion. Cromolyn and quercetin pretreatment significantly inhibited permeability changes, but did not influence pHi and morphological alterations induced by ischemia-reperfusion. Dexamethasone pretreatment did not influence the number of mast cells, however, the degree of mast cell degranulation and the degree of mucosal damage decreased. These results demonstrate that mast cells or mast cell-induced reactions contribute to the mucosal permeability alterations and barrier lesions during reperfusion, but play a minor role in reperfusion-induced structural injury.
authors.affiliation: Institute of Experimental Surgery, Albert Szent-Györgyi Medical University, Szeged, Hungary.
authors.forename: A
authors.initials: A
authors.lastname: Szabó
authors.forename: M
authors.initials: M
authors.lastname: Boros
authors.forename: J
authors.initials: J
authors.lastname: Kaszaki
authors.forename: S
authors.initials: S
authors.lastname: Nagy
mesh_terms: D000818:Animals; D018927:Anti-Asthmatic Agents / Q000494:pharmacology; D002452:Cell Count; D015550:Cell Degranulation; D002462:Cell Membrane / Q000187:drug effects; D003287:Contrast Media / Q000493:pharmacokinetics; D004205:Cromolyn Sodium / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004285:Dogs; D019793:Fluorescein / Q000493:pharmacokinetics; D005938:Glucocorticoids / Q000494:pharmacology; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000473:pathology; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D008407:Mast Cells / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D010539:Permeability; D011794:Quercetin / Q000494:pharmacology; D015427:Reperfusion Injury / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D014655:Vascular Resistance
chemical_list: D018927:Anti-Asthmatic Agents; D003287:Contrast Media; D005938:Glucocorticoids; D003907:Dexamethasone; D011794:Quercetin; D004205:Cromolyn Sodium; D019793:Fluorescein