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Physiol Rep. 2017 Jul;5(13). pii: e13231. doi: 10.14814/phy2.13231.

Early sepsis does not stimulate reactive oxygen species production and does not reduce cardiac function despite an increased inflammation status.

Author information

1
INRA, UMR 1019 Nutrition Humaine, Clermont-Ferrand Cedex 1, France.
2
Laboratoire de Bioénergétique Fondamentale et Appliquée, INSERM U1055, Université Joseph Fourier, Grenoble, France.
3
Department of Medical Biochemistry and Molecular Biology, CHU Clermont-Ferrand, Clermont-Ferrand, France.
4
Department of Clinical Research and Innovation, CHU Clermont-Ferrand, Clermont-Ferrand, France.
5
Heart Surgery Department, G. Montpied Hospital, Clermont-Ferrand University Hospital, Clermont-Ferrand, France.
6
INRA, UMR 1019 Nutrition Humaine, Clermont-Ferrand Cedex 1, France luc.demaison@clermont.inra.fr.

Abstract

If it is sustained for several days, sepsis can trigger severe abnormalities of cardiac function which leads to death in 50% of cases. This probably occurs through activation of toll-like receptor-9 by bacterial lipopolysaccharides and overproduction of proinflammatory cytokines such as TNF-α and IL-1β In contrast, early sepsis is characterized by the development of tachycardia. This study aimed at determining the early changes in the cardiac function during sepsis and at finding the mechanism responsible for the observed changes. Sixty male Wistar rats were randomly assigned to two groups, the first one being made septic by cecal ligation and puncture (sepsis group) and the second one being subjected to the same surgery without cecal ligation and puncture (sham-operated group). The cardiac function was assessed in vivo and ex vivo in standard conditions. Several parameters involved in the oxidative stress and inflammation were determined in the plasma and heart. As evidenced by the plasma level of TNF-α and gene expression of IL-1β and TNF-α in the heart, inflammation was developed in the sepsis group. The cardiac function was also slightly stimulated by sepsis in the in vivo and ex vivo situations. This was associated with unchanged levels of oxidative stress, but several parameters indicated a lower cardiac production of reactive oxygen species in the septic group. In conclusion, despite the development of inflammation, early sepsis did not increase reactive oxygen species production and did not reduce myocardial function. The depressant effect of TNF-α and IL-1β on the cardiac function is known to occur at very high concentrations. The influence of low- to moderate-grade inflammation on the myocardial mechanical behavior must thus be revisited.

KEYWORDS:

Contractility; heart; oxidative stress; sepsis

PMID:
28684640
PMCID:
PMC5506518
DOI:
10.14814/phy2.13231
[Indexed for MEDLINE]
Free PMC Article

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