title: Fenoldopam--but not dopamine--selectively increases gastric mucosal oxygenation in dogs.
abstract: OBJECTIVE
  To compare the effects of fenoldopam and dopamine on gastric mucosal and systemic oxygenation, and to identify the receptors involved.
  
  
  METHODS
  Randomized controlled animal study.
  
  
  METHODS
  University research department of experimental anesthesiology. SUBJECTS Seven anesthetized dogs with chronically implanted ultrasound flow probes around the pulmonary artery for continuous measurement of cardiac output.
  
  
  METHODS
  On different days, the dogs received in random order either the selective DA(1)-agonist fenoldopam (0.1 and 1.0 microg x kg-1.= x min-1, with or without DA(1)-blocker pretreatment), dopamine (2.5 and 5.0 microg.kg-1 x min-1, with or without alpha(1)-blocker pretreatment), or saline (control).
  
  
  RESULTS
  We continuously measured regional microvascular hemoglobin oxygen saturation (muHbO(2)) in gastric mucosa by reflectance spectrophotometry, and systemic oxygen delivery. Fenoldopam increased gastric mucosal muHbO(2) by approximately 20%, and this effect was prevented by selective DA(1)-receptor blockade. In contrast, dopamine neither alone nor during alpha(1)-blockade altered muHbO(2). With respect to systemic measures of oxygen transport, fenoldopam had negligible effects, whereas dopamine (with and without alpha(1)-blocker pretreatment) dose-dependently increased cardiac output and systemic oxygen delivery by approximately 30%.
  
  
  CONCLUSIONS
  Fenoldopam dose-dependently increased microvascular oxygenation of the gastric mucosa without changing systemic oxygen transport, i.e., this drug acted selectively on the splanchnic mucosa. The increase in gastric mucosal oxygenation was mediated by DA(1)-receptors. In contrast, dopamine markedly increased systemic oxygen transport, but did not affect microvascular oxygenation of gastric mucosa. This lacking effect on gastric mucosal oxygenation was not caused by alpha(1)-mediated vasoconstriction. The regional effects of both catecholamines could not be deduced from systemic hemodynamics and oxygenation.
authors.affiliation: Department of Anesthesiology, University Hospital of Dusseldorf, Germany.
authors.forename: Lothar A
authors.initials: LA
authors.lastname: Schwarte
authors.forename: Olaf
authors.initials: O
authors.lastname: Picker
authors.forename: Achim W
authors.initials: AW
authors.lastname: Schindler
authors.forename: Artur
authors.initials: A
authors.lastname: Fournell
authors.forename: Thomas W L
authors.initials: TW
authors.lastname: Scheeren
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D004298:Dopamine / Q000494:pharmacology*; D018491:Dopamine Agonists / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D018818:Fenoldopam / Q000494:pharmacology*; D005753:Gastric Mucosa / Q000098:blood supply*; D008297:Male; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption / Q000187:drug effects*; D010108:Oxyhemoglobins / Q000378:metabolism; D011224:Prazosin / Q000494:pharmacology; D017447:Receptors, Dopamine D1 / Q000819:agonists
chemical_list: D000317:Adrenergic alpha-Antagonists; D001552:Benzazepines; D018491:Dopamine Agonists; D010108:Oxyhemoglobins; D017447:Receptors, Dopamine D1; D018818:Fenoldopam; D010100:Oxygen; D004298:Dopamine; D011224:Prazosin