Hypertonic sodium lactate improves microcirculation, modulates inflammation, and preserves vascular reactivity in a rat model of sepsis: in vivo and ex vivo evidence.

Authors

Eva Correia, Thomas Maudhuizon, Antoine Hérault, Soumeya Bekri, Eric Fontaine, Jérémy Bellien, Paul Mulder, Fabienne Tamion, Emmanuel Besnier

Published in

Intensive care medicine experimental. Volume 14. Issue 1. Sep 20, 2026. Epub Sep 20, 2026.

Abstract

Hypertonic sodium lactate (HSL) has demonstrated beneficial effects in experimental sepsis, improving hemodynamics, modulating inflammation, and supporting cellular metabolism. Nevertheless, prior studies have not specifically addressed microcirculation, despite its critical impairment during sepsis and the absence of targeted therapies. We evaluated the therapeutic effects of HSL in a in vivo resuscitated rat model (Male wistars) of cecal ligation and puncture (CLP), with a particular focus on microcirculatory function, followed by ex vivo investigation of sodium lactate on vascular reactivity.
10 h after CLP rats were infused with 0.9% NaCl or 11.2% HSL for 18 h before exploration. No difference was observed on arterial pressure, echocardiography and pressure-volume loops. HSL improved mesenteric perfusion (1126 [923-1300] vs. 816.5 [692-919] Perfusion Unit, p = 0.012) and TNF-α plasma levels (26.2 [22.8-37.1] vs. 42.6 [32.6-47.3] pg/mL, p = 0.001). Ex vivo, mesenteric artery reactivity experiments from healthy rats was tested with or without LPS-stimulation and glucose deprivation. Lactate dose-dependently restored LPS-impaired vasoconstriction, showing an independent effect on small arteries. In glucose deprivation conditions, HSL was able to restore vascular reactivity in normal or LPS-stimulated arteries.
HSL specifically improved microcirculation and reduced systemic inflammation in septic rats. Moreover, lactate may act as an alternative to glucose in deprivation conditions. These benefits support its translational potential as a resuscitation fluid in sepsis.

PMID:
42763846
Bibliographic data and abstract were imported from PubMed on 21 Sep 2026.

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