Splanchnic vasoconstriction by angiotensin II is arterial pressure dependent

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...

Full description

Saved in:
Bibliographic Details
Published inActa anaesthesiologica Scandinavica Vol. 46; no. 1; pp. 57 - 63
Main Authors Broomé, M., Åneman, A., Lehtipalo, S., Arnerlöv, C., Johansson, G., Winsö, O., Biber, B.
Format Journal Article
LanguageEnglish
Published Copenhagen Munksgaard International Publishers 01.01.2002
Blackwell
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary: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 μg · 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. Conclusion: 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.
Bibliography:ark:/67375/WNG-MSRT109W-0
ArticleID:aas1o049
istex:A626FD9229A6C21C0CF3CBA42BA8D05D1FEEA0D4
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0001-5172
1399-6576
1399-6576
DOI:10.1034/j.1399-6576.2002.460110.x