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Molar Sodium Lactate Attenuates the Severity of Postcardiac Arrest Syndrome: A Preclinical Study

Authors :
Gabriel Bidaux
Laurent Argaud
Louis Kreitmann
Neven Stevic
Martin Cour
Michel Ovize
Laurent Desmurs
Joseph Loufouat
CarMeN, laboratoire
Hôpital Edouard Herriot [CHU - HCL]
Hospices Civils de Lyon (HCL)
Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN)
Université Claude Bernard Lyon 1 (UCBL)
Université de Lyon-Université de Lyon-Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)
Source :
Critical Care Medicine, Critical Care Medicine, 2021, 50 (1), pp.E71-E79. ⟨10.1097/ccm.0000000000005233⟩, Critical Care Medicine, Lippincott, Williams & Wilkins, 2021, 50 (1), pp.E71-E79. ⟨10.1097/ccm.0000000000005233⟩
Publication Year :
2021
Publisher :
Ovid Technologies (Wolters Kluwer Health), 2021.

Abstract

International audience; OBJECTIVES: To determine whether continuous IV infusion of molar sodium lactate would limit cardiac arrest-induced neurologic injury and cardiovascular failure. DESIGN: Randomized blinded study (animal model). SETTING: University animal research facility. SUBJECTS: Twenty-four adult male "New Zealand White" rabbits. INTERVENTIONS: Anesthetized rabbits underwent 12.5 minutes of asphyxial cardiac arrest and were randomized to receive either normal saline (control group, n = 12) or molar sodium lactate (molar sodium lactate group, n = 12) at a rate of 5 mL/kg/hr during the whole 120-minute reperfusion period. MEASUREMENTS AND MAIN RESULTS: Pupillary reactivity (primary outcome), levels of S100β protein, in vitro brain mitochondria functions, cardiovascular function, and fluid balance were assessed. Molar sodium lactate reduced brain injury, with a higher proportion of animals exhibiting pupillary reactivity to light (83% vs 25% in the CTRL group, p = 0.01) and lower S100β protein levels (189 ± 42 vs 412 ± 63 pg/mL, p \textless 0.01) at the end of the protocol. Molar sodium lactate significantly prevented cardiac arrest-induced decrease in oxidative phosphorylation and mitochondrial calcium-retention capacity compared with controls. At 120 minutes of reperfusion, survival did not significantly differ between the groups (10/12, 83% in the molar sodium lactate group vs nine of 12, 75% in the control group; p \textgreater 0.99), but hemodynamics were significantly improved in the molar sodium lactate group compared with the control group (higher mean arterial pressure [49 ± 2 vs 29 ± 3 mm Hg; p \textless 0.05], higher cardiac output [108 ± 4 vs 58 ± 9 mL/min; p \textless 0.05], higher left ventricle surface shortening fraction [38% ± 3% vs 19% ± 3%; p \textless 0.05], and lower left ventricular end-diastolic pressure [3 ± 1 vs 8 ± 2 mm Hg; p \textless 0.01]). While fluid intake was similar in both groups, fluid balance was higher in control animals (11 ± 1 mL/kg) than that in molar sodium lactate-treated rabbits (1 ± 3 mL/kg; p \textless 0.01) due to lower diuresis. CONCLUSIONS: Molar sodium lactate was effective in limiting the severity of the postcardiac arrest syndrome. This preclinical study opens up new perspectives for the treatment of cardiac arrest.

Details

ISSN :
00903493 and 15300293
Volume :
50
Database :
OpenAIRE
Journal :
Critical Care Medicine
Accession number :
edsair.doi.dedup.....6127dd6f0868dc0f3135a1ab2f2701bb