Hypertonic sodium lactate infusion reduces vasopressor requirements and biomarkers of brain and cardiac injury after experimental cardiac arrest.


Journal

Critical care (London, England)
ISSN: 1466-609X
Titre abrégé: Crit Care
Pays: England
ID NLM: 9801902

Informations de publication

Date de publication:
22 04 2023
Historique:
received: 08 03 2023
accepted: 19 04 2023
medline: 25 4 2023
pubmed: 23 4 2023
entrez: 22 04 2023
Statut: epublish

Résumé

Prognosis after resuscitation from cardiac arrest (CA) remains poor, with high morbidity and mortality as a result of extensive cardiac and brain injury and lack of effective treatments. Hypertonic sodium lactate (HSL) may be beneficial after CA by buffering severe metabolic acidosis, increasing brain perfusion and cardiac performance, reducing cerebral swelling, and serving as an alternative energetic cellular substrate. The aim of this study was to test the effects of HSL infusion on brain and cardiac injury in an experimental model of CA. After a 10-min electrically induced CA followed by 5 min of cardiopulmonary resuscitation maneuvers, adult swine (n = 35) were randomly assigned to receive either balanced crystalloid (controls, n = 11) or HSL infusion started during cardiopulmonary resuscitation (CPR, Intra-arrest, n = 12) or after return of spontaneous circulation (Post-ROSC, n = 11) for the subsequent 12 h. In all animals, extensive multimodal neurological and cardiovascular monitoring was implemented. All animals were treated with targeted temperature management at 34 °C. Thirty-four of the 35 (97.1%) animals achieved ROSC; one animal in the Intra-arrest group died before completing the observation period. Arterial pH, lactate and sodium concentrations, and plasma osmolarity were higher in HSL-treated animals than in controls (p < 0.001), whereas potassium concentrations were lower (p = 0.004). Intra-arrest and Post-ROSC HSL infusion improved hemodynamic status compared to controls, as shown by reduced vasopressor requirements to maintain a mean arterial pressure target > 65 mmHg (p = 0.005 for interaction; p = 0.01 for groups). Moreover, plasma troponin I and glial fibrillary acid protein (GFAP) concentrations were lower in HSL-treated groups at several time-points than in controls. In this experimental CA model, HSL infusion was associated with reduced vasopressor requirements and decreased plasma concentrations of measured biomarkers of cardiac and cerebral injury.

Identifiants

pubmed: 37087454
doi: 10.1186/s13054-023-04454-1
pii: 10.1186/s13054-023-04454-1
pmc: PMC10122448
doi:

Substances chimiques

Sodium Lactate TU7HW0W0QT
Vasoconstrictor Agents 0
Biomarkers 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

161

Informations de copyright

© 2023. The Author(s).

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Auteurs

Filippo Annoni (F)

Department of Intensive Care, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium. filippo.annoni@erasme.ulb.ac.be.
Experimental Laboratory of Intensive Care, Free University of Brussels, Brussels, Belgium. filippo.annoni@erasme.ulb.ac.be.

Fuhong Su (F)

Department of Intensive Care, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium.
Experimental Laboratory of Intensive Care, Free University of Brussels, Brussels, Belgium.

Lorenzo Peluso (L)

Department of Intensive Care, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium.
Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, Italy.
Department of Anesthesiology and Intensive Care, Humanitas Gavazzeni, Via M Gavazzeni 21, 24125, Bergamo, Italy.

Ilaria Lisi (I)

Laboratory of Traumatic Brain Injury and Neuroprotection, Department of Acute Brain Injury, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy.

Enrico Caruso (E)

Laboratory of Traumatic Brain Injury and Neuroprotection, Department of Acute Brain Injury, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy.

Francesca Pischiutta (F)

Laboratory of Traumatic Brain Injury and Neuroprotection, Department of Acute Brain Injury, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy.

Elisa Gouvea Bogossian (E)

Department of Intensive Care, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium.

Bruno Garcia (B)

Department of Intensive Care, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium.
Experimental Laboratory of Intensive Care, Free University of Brussels, Brussels, Belgium.

Hassane Njimi (H)

Department of Intensive Care, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium.

Jean-Louis Vincent (JL)

Department of Intensive Care, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium.

Nicolas Gaspard (N)

Department of Neurology, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium.
Neurology Department, School of Medicine, Yale University, New Haven, CT, USA.

Lorenzo Ferlini (L)

Department of Neurology, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium.

Jacques Creteur (J)

Department of Intensive Care, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium.

Elisa R Zanier (ER)

Laboratory of Traumatic Brain Injury and Neuroprotection, Department of Acute Brain Injury, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy.

Fabio Silvio Taccone (FS)

Department of Intensive Care, Erasme Hospital, Lennik Road 808, 1070, Brussels, Belgium.
Experimental Laboratory of Intensive Care, Free University of Brussels, Brussels, Belgium.

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Classifications MeSH