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Cellular mechanisms of myocardial depression in porcine septic shock

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11140%2F18%3A10376370" target="_blank" >RIV/00216208:11140/18:10376370 - isvavai.cz</a>

  • Result on the web

    <a href="https://www.frontiersin.org/articles/10.3389/fphys.2018.00726/full" target="_blank" >https://www.frontiersin.org/articles/10.3389/fphys.2018.00726/full</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3389/fphys.2018.00726" target="_blank" >10.3389/fphys.2018.00726</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Cellular mechanisms of myocardial depression in porcine septic shock

  • Original language description

    The complex pathogenesis of sepsis and septic shock involves myocardial depression, the pathophysiology of which, however, remains unclear. In this study, cellular mechanisms of myocardial depression were addressed in a clinically relevant, large animal (porcine) model of sepsis and septic shock. Sepsis was induced by fecal peritonitis in 8 anesthetized, mechanically ventilated, and instrumented pigs of both sexes and continued for 24 hours. In 8 control pigs, an identical experiment but without sepsis induction was performed. In vitro analysis of cardiac function included measurements of action potentials and contractions in the right ventricle trabeculae, measurements of sarcomeric contractions, calcium transients and calcium current in isolated cardiac myocytes, and analysis of mitochondrial respiration by ultrasensitive oxygraphy. Increased values of modified Sequential Organ Failure Assessment (SOFA) score and serum lactate levels documented the development of sepsis/septic shock, accompanied by hyperdynamic circulation with high heart rate, increased cardiac output, peripheral vasodilation, and decreased stroke volume. In septic trabeculae, action potential duration was shortened and contraction force reduced. In septic cardiac myocytes, sarcomeric contractions, calcium transients, and L-type calcium current were all suppressed. Similar relaxation trajectory of the intracellular calcium-cell length phase-plane diagram indicated unchanged calcium responsiveness of myofilaments. Mitochondrial respiration was diminished through inhibition of Complex II and Complex IV. Defective calcium handling with reduced calcium current and transients, together with inhibition of mitochondrial respiration, appears to represent the dominant cellular mechanisms of myocardial depression in porcine septic shock.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30105 - Physiology (including cytology)

Result continuities

  • Project

    <a href="/en/project/GA15-15716S" target="_blank" >GA15-15716S: The role of autonomic nervous system in sepsis development</a><br>

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2018

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Frontiers in Physiology

  • ISSN

    1664-042X

  • e-ISSN

  • Volume of the periodical

    9

  • Issue of the periodical within the volume

    June

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    11

  • Pages from-to

  • UT code for WoS article

    000434983900001

  • EID of the result in the Scopus database

    2-s2.0-85048536577