Micro-lightguide spectrophotometry assessment of hepatic and intestinal microcirculation in endotoxemic rats during intravenous treatment with angiotensin II

dc.contributor.authorSchmidt, Götz
dc.contributor.authorPitz, Laurenz
dc.contributor.authorMarkmann, Melanie
dc.contributor.authorSchneck, Emmanuel
dc.contributor.authorSander, Michael
dc.contributor.authorKoch, Christian
dc.contributor.authorEdinger, Fabian
dc.date.accessioned2024-10-01T13:06:26Z
dc.date.available2024-10-01T13:06:26Z
dc.date.issued2023
dc.description.abstractIntroduction: During septic shock, impairment of microcirculation leads to enhanced permeability of intestinal mucosa triggered by generalized vasodilation and capillary leak. Intravenous angiotensin II (AT-II) has been approved for the treatment of septic shock; however, no in-vivo data exist on the influence of AT-II on hepatic and intestinal microcirculation. Material and methods: Sixty male Lewis rats were randomly assigned to six study groups (each n = 10): sham, lipopolysaccharide-induced septic shock, therapy with low- or high-dose AT-II (50 or 100 ng/kg/min, respectively), and septic shock treated with low- or high-dose AT-II. After median laparotomy, hepatic and intestinal microcirculation measures derived from micro-lightguide spectrophotometry were assessed for 3 h and included oxygen saturation (SO2), relative blood flow (relBF) and relative hemoglobin level (relHb). Hemodynamic measurements were performed using a left ventricular conductance catheter, and blood samples were taken hourly to analyze blood gasses and systemic cytokines. Results: AT-II increased mean arterial pressure in a dose-dependent manner in both septic and non-septic animals (p < 0.001). Lower hepatic and intestinal SO2 (both p < 0.001) were measured in animals without endotoxemia who received high-dose AT-II treatment, however, significantly impaired cardiac output was also reported in this group (p < 0.001). In endotoxemic rats, hepatic relBF and relHb were comparable among the treatment groups; however, hepatic SO2 was reduced during low- and high-dose AT-II treatment (p < 0.001). In contrast, intestinal SO2 remained unchanged despite treatment with AT-II. Intestinal relBF (p = 0.028) and interleukin (IL)-10 plasma levels (p < 0.001) were significantly elevated during treatment with high-dose AT-II compared with low-dose AT-II. Conclusions: A dose-dependent decrease of hepatic and intestinal microcirculation during therapy with AT-II in non-septic rats was observed, which might have been influenced by a corresponding reduction in cardiac output due to elevated afterload. While hepatic microcirculation was reduced during endotoxemia, no evidence for a reduction in intestinal microcirculation facilitated by AT-II was found. In contrast, both intestinal relBF and anti-inflammatory IL-10 levels were increased during high-dose AT-II treatment.en
dc.identifier.urihttps://jlupub.ub.uni-giessen.de/handle/jlupub/19544
dc.identifier.urihttps://doi.org/10.22029/jlupub-18902
dc.language.isoen
dc.rightsNamensnennung 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subject.ddcddc:610
dc.titleMicro-lightguide spectrophotometry assessment of hepatic and intestinal microcirculation in endotoxemic rats during intravenous treatment with angiotensin II
dc.typearticle
local.affiliationFB 11 - Medizin
local.source.articlenumber106588
local.source.epage12
local.source.journaltitleEuropean journal of pharmaceutical sciences
local.source.spage1
local.source.urihttps://doi.org/10.1016/j.ejps.2023.106588
local.source.volume191

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