title: Splanchnic vasoconstriction by angiotensin II is arterial pressure dependent.
abstract: BACKGROUND
  Our hypothesis was that splanchnic vasoconstriction by exogenous angiotensin II (Ang II) is significantly potentiated by local mechanisms increasing vasomotor tone and that splanchnic tissue oxygenation during administration of Ang II is perfusion pressure dependent. The aim was to study local splanchnic circulatory effects and tissue oxygenation during intravenous infusion of Ang II at different levels of regional arterial driving pressure in a whole-body large animal model.
  
  
  METHODS
  Ang II was infused in incremental doses (0-200 microg x h-1) in anaesthetised instrumented pigs (n=8). Mean superior mesenteric arterial pressure (PSMA) was adjusted by a local variable perivascular occluder. Perivascular ultrasound and laser-Doppler flowmetry were used for measurements of mesenteric venous blood flow and superficial intestinal blood flow, respectively. Intestinal oxygenation was evaluated by oxygen tissue tension (PtiO2) and lactate fluxes.
  
  
  RESULTS
  Ang II produced prominent and dose-dependent increases in mesenteric vascular resistance (RSMA) when the intestine was exposed to systemic arterial pressure, but Ang II increased RSMA only minimally when PSMA was artificially kept constant at a lower level (50 mmHg) by the occluder. Although Ang II decreased PtiO2 at a PSMA of 50 mmHg, splanchnic lactate production was not observed.
  
  
  CONCLUSIONS
  We demonstrate that splanchnic vasoconstriction by exogenous Ang II is dependent on arterial driving pressure, suggesting significant potentiation through autoregulatory increases in vasomotor tone. Intestinal hypoxaemia does not seem to occur during short-term infusion of Ang II in doses that significantly increases systemic arterial pressure.
authors.affiliation: Dept. of Surgical and Perioperative Science, Anaesthesiology and Intensive Care, Umeå University Hospital, Umeå, Sweden. michael.broome.us@vll.se
authors.forename: M
authors.initials: M
authors.lastname: Broomé
authors.forename: A
authors.initials: A
authors.lastname: Aneman
authors.forename: S
authors.initials: S
authors.lastname: Lehtipalo
authors.forename: C
authors.initials: C
authors.lastname: Arnerlöv
authors.forename: G
authors.initials: G
authors.lastname: Johansson
authors.forename: O
authors.initials: O
authors.lastname: Winsö
authors.forename: B
authors.initials: B
authors.lastname: Biber
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D007583:Jejunum / Q000098:blood supply / Q000378:metabolism; D017078:Laser-Doppler Flowmetry; D017538:Mesenteric Artery, Superior / Q000502:physiology; D008642:Mesenteric Veins / Q000502:physiology; D010100:Oxygen / Q000378:metabolism; D010101:Oxygen Consumption; D013152:Splanchnic Circulation / Q000187:drug effects / Q000502:physiology*; D013552:Swine; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D010100:Oxygen