EARLY DECREASED RESPIRATORY CHAIN CAPACITY IN RESUSCITATED EXPERIMENTAL SEPSIS IS A MAJOR CONTRIBUTOR TO LACTATE PRODUCTION.
Journal
Shock (Augusta, Ga.)
ISSN: 1540-0514
Titre abrégé: Shock
Pays: United States
ID NLM: 9421564
Informations de publication
Date de publication:
01 09 2023
01 09 2023
Historique:
medline:
13
9
2023
pubmed:
7
8
2023
entrez:
7
8
2023
Statut:
ppublish
Résumé
Background : Increased plasma lactate levels in patients with sepsis may be due to insufficient oxygen delivery, but mitochondrial dysfunction or accelerated glycolysis may also contribute. We studied the effect of the latter on muscle metabolism by using microdialysis in a sepsis model with sustained oxygen delivery and decreased energy consumption or mitochondrial blockade. Methods : Pigs were subjected to continuous Escherichia coli infusion (sepsis group, n = 12) or saline infusion (sham group, n = 4) for 3 h. Protocolized interventions were applied to normalize the oxygen delivery and blood pressure. Microdialysis catheters were used to monitor muscle metabolism (naïve). The same catheters were used to block the electron transport chain with cyanide or the Na + /K + -ATPase inhibitor, ouabain locally. Results: All pigs in the sepsis group had positive blood cultures and a Sequential Organ Failure Assessment score increase by at least 2, fulfilling the sepsis criteria. Plasma lactate was higher in the sepsis group than in the sham group ( P < 0.001), whereas muscle glucose was lower in the sepsis group ( P < 0.01). There were no changes in muscle lactate levels over time but lactate to pyruvate ratio (LPR) was elevated in the sepsis versus the sham group ( P < 0.05). Muscle lactate, LPR, and glutamate levels were higher in the sepsis group than in the sham group in the cyanide catheters ( P < 0.001, all comparisons) and did not normalize in the former group. Conclusions: In this experimental study on resuscitated sepsis, we observed increased aerobic metabolism and preserved mitochondrial function. Sepsis and electron transport chain inhibition led to increased LPR, suggesting a decreased mitochondrial reserve capacity in early sepsis.
Identifiants
pubmed: 37548644
doi: 10.1097/SHK.0000000000002190
pii: 00024382-990000000-00252
doi:
Substances chimiques
Lactic Acid
33X04XA5AT
Oxygen
S88TT14065
Cyanides
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
461-468Informations de copyright
Copyright © 2023 by the Shock Society.
Déclaration de conflit d'intérêts
The authors report no conflicts of interest.
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