title: Gastric mucosal blood flow regulation in response to different stimuli.
abstract: We compared changes in gastric mucosal blood flow (GMBF) and left gastric artery blood flow (LGABF) in response to pharmacological, physiological, and pathological stimuli. GMBF and LGABF were measured by the hydrogen gas clearance and perivascular ultrasonic transit time techniques, respectively, under baseline conditions and following intravenous infusion of vasopressin or pentagastrin, isovolemic hemodilution, or gastric perfusion with HCl-taurocholate. Blood flow changes following vasopressin or hemodilution were significantly larger in the left gastric artery than in the gastric mucosa. In contrast, the increment in blood flow associated with pentagastrin-stimulated acid secretion was significantly greater in the gastric mucosa than in the extramural artery. Barrier disruption with acid-taurocholate induced similar changes in both measurement sites. The gastric hyperemia induced by either mechanism was significantly attenuated by blockade of NO synthesis. These data demonstrate that although functional changes in GMBF are primarily supported by changes in blood flow at the extramural gastric arteries, the gastric mucosal microvasculature is also under the influence of independent local control mechanisms.
authors.affiliation: Department of Gastroenterology, University of La Laguna in Tenerife, Spain.
authors.forename: A
authors.initials: A
authors.lastname: Méndez
authors.forename: M
authors.initials: M
authors.lastname: Casadevall
authors.forename: C H
authors.initials: CH
authors.lastname: Wachter
authors.forename: J I
authors.initials: JI
authors.lastname: Elizalde
authors.forename: M
authors.initials: M
authors.lastname: Del Rivero
authors.forename: A
authors.initials: A
authors.lastname: Heinemann
authors.forename: P
authors.initials: P
authors.lastname: Holzer
authors.forename: E
authors.initials: E
authors.lastname: Quintero
authors.forename: J M
authors.initials: JM
authors.lastname: Piqué
mesh_terms: D000740:Anemia / Q000503:physiopathology; D000818:Animals; D001158:Arteries / Q000000981:diagnostic imaging; D005260:Female; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000098:blood supply*; D006438:Hemodilution; D006859:Hydrogen; D006940:Hyperemia / Q000139:chemically induced / Q000503:physiopathology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000502:physiology; D010418:Pentagastrin / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D013270:Stomach / Q000098:blood supply; D013656:Taurocholic Acid / Q000494:pharmacology; D014463:Ultrasonography; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014667:Vasopressins; D009569:Nitric Oxide; D013656:Taurocholic Acid; D006859:Hydrogen; D010418:Pentagastrin; D019331:NG-Nitroarginine Methyl Ester