Skip to main content

Norepinephrine versus angiotensin II in septic shock: effects on isolated kidney, heart and liver mitochondrial respiration

Introduction

Mitochondrial dysfunction has been proposed to influence organ function and outcome in sepsis. Both vasopressor agents norepinephrine and angiotensin II can interfere with mitochondrial function. The aim of this study was to compare mitochondrial respiration after exposure of septic animals to either of these two drugs.

Methods

In 16 anesthetized pigs, evolving septic shock after 12 hours of fecal peritonitis was randomly treated with either norepinephrine (0.8 ± 0.6 μg/kg/minute; mean ± SD) or angiotensin II (0.31 ± 0.37 μg/kg/minute; n = 8, each) and fluids for 48 hours. Organs were harvested at the end of the experiment, and mitochondria isolated by tissue homogenization and differential centrifugation. Mitochondrial oxygen consumption (VO2) was measured by high-resolution respirometry (Oroboros Instruments, Innsbruck, Austria). Groups were compared using Mann-Whitney U test. In addition, mitochondrial respiration was also compared to a similarly instrumented control group without fecal peritonitis (n = 8; Kruskal-Wallis test).

Results

Achieved blood pressure levels and cardiac output were not different between the two septic groups, and both groups received the same amount of fluids (norepinephrine: 1.6 ± 0.5 ml/kg/hour, angiotensin II: 1.3 ± 0.8 ml/kg/hour; P = NS). Compared to controls, mitochondrial VO2 was not different in septic animals. The only difference between the two septic groups was higher renal Complex I, State 4 respiration in norepinephrine-treated (median (range): 309 (164 to 415) pmol/(second*mg)) versus angiotensin-II-treated animals (210 (89 to 273) pmol/(second*mg); P = 0.05).

Conclusion

We found no significant effects of septic shock treated with either angiotensin II or norepinephrine and fluids on mitochondrial function, under similar hemodynamic conditions. Hepatic, renal and myocardial respiration of the measured mitochondrial complexes did not significantly differ between the two treatment groups, except for renal Complex I, State 4 respiration.

Author information

Affiliations

Authors

Corresponding author

Correspondence to V Jeger.

Rights and permissions

This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

About this article

Cite this article

Jeger, V., Vuda, M., Correa, T. et al. Norepinephrine versus angiotensin II in septic shock: effects on isolated kidney, heart and liver mitochondrial respiration. Crit Care 16, P196 (2012). https://doi.org/10.1186/cc10803

Download citation

Keywords

  • Norepinephrine
  • Septic Shock
  • Mitochondrial Function
  • Mitochondrial Respiration
  • Blood Pressure Level