IMPAIRMENT OF MITOCHONDRIAL FUNCTION IN MURINE SEPSIS SURVIVORS

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Abstract Sepsis, a life-threatening condition accompanied by profound systemic inflammation, is a serious problem among the aging population as both susceptibility and mortality increase dramatically with age. Among survivors, >70% report muscle weakness for years after hospital discharge. Published studies aimed at elucidating the underlying mechanism for this phenomenon have been limited to analysis during sepsis due to the lack of an appropriate model (i.e. models are too severe and cause early death or are too mild to induce long-term weakness). Despite this limitation, these studies have consistently observed mitochondrial dysfunction during sepsis. The objective of the current study was to determine if mitochondria remained dysfunctional weeks after recovery from severe sepsis. Experimental sepsis was induced in 16-month-old mice by cecal slurry injection in combination with ICU-like interventions (antibiotic and fluid resuscitation). Two weeks later, mice were euthanized and mitochondria from the tibialis anterior (TA; fast-twitch) and soleus (slow-twitch) muscles were isolated and subjected to respiration analysis using Seahorse Biosciences technology. The maximum ATP phosphorylation rate was significantly reduced in the TA of survivors however State IV was unchanged, suggestive of increased electron leakage. State V-driven-Complex I activity was also reduced. No signif

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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