Hypertonic sodium lactate improves microcirculation, cardiac function, and inflammation in a rat model of sepsis

Crit Care. 2020 Jun 16;24(1):354. doi: 10.1186/s13054-020-03083-2.

Abstract

Background: Hypertonic sodium lactate (HSL) may be of interest during inflammation. We aimed to evaluate its effects during experimental sepsis in rats (cecal ligation and puncture (CLP)).

Methods: Three groups were analyzed (n = 10/group): sham, CLP-NaCl 0.9%, and CLP-HSL (2.5 mL/kg/h of fluids for 18 h after CLP). Mesenteric microcirculation, echocardiography, cytokines, and biochemical parameters were evaluated. Two additional experiments were performed for capillary leakage (Evans blue, n = 5/group) and cardiac hemodynamics (n = 7/group).

Results: HSL improved mesenteric microcirculation (CLP-HSL 736 [407-879] vs. CLP-NaCl 241 [209-391] UI/pixel, p = 0.0006), cardiac output (0.34 [0.28-0.43] vs. 0.14 [0.10-0.18] mL/min/g, p < 0.0001), and left ventricular fractional shortening (55 [46-73] vs. 39 [33-52] %, p = 0.009). HSL also raised dP/dtmax slope (6.3 [3.3-12.1] vs. 2.7 [2.0-3.9] 103 mmHg/s, p = 0.04), lowered left ventricular end-diastolic pressure-volume relation (1.9 [1.1-2.3] vs. 3.0 [2.2-3.7] RVU/mmHg, p = 0.005), and reduced Evans blue diffusion in the gut (37 [31-43] vs. 113 [63-142], p = 0.03), the lung (108 [82-174] vs. 273 [222-445], p = 0.006), and the liver (24 [14-37] vs. 70 [50-89] ng EB/mg, p = 0.04). Lactate and 3-hydroxybutyrate were higher in CLP-HSL (6.03 [3.08-10.30] vs. 3.19 [2.42-5.11] mmol/L, p = 0.04; 400 [174-626] vs. 189 [130-301] μmol/L, p = 0.03). Plasma cytokines were reduced in HSL (IL-1β, 172 [119-446] vs. 928 [245-1470] pg/mL, p = 0.004; TNFα, 17.9 [12.5-50.3] vs. 53.9 [30.8-85.6] pg/mL, p = 0.005; IL-10, 352 [267-912] vs. 905 [723-1243] pg/mL) as well as plasma VEGF-A (198 [185-250] vs. 261 [250-269] pg/mL, p = 0.009).

Conclusions: Hypertonic sodium lactate fluid protects against cardiac dysfunction, mesenteric microcirculation alteration, and capillary leakage during sepsis and simultaneously reduces inflammation and enhances ketone bodies.

Keywords: Heart failure; Metabolism; Microcirculation; Sepsis; Sodium lactate.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Disease Models, Animal
  • Echocardiography / methods
  • Endothelial Growth Factors / analysis
  • Endothelial Growth Factors / blood
  • Heart Function Tests / methods
  • Hypertonic Solutions / therapeutic use
  • Inflammation* / drug therapy
  • Inflammation* / physiopathology
  • Interleukin-10 / analysis
  • Interleukin-10 / blood
  • Interleukin-1beta / analysis
  • Interleukin-1beta / blood
  • Microcirculation* / drug effects
  • Microcirculation* / physiology
  • Prospective Studies
  • Rats
  • Sepsis* / drug therapy
  • Sepsis* / physiopathology
  • Sodium Lactate* / pharmacology
  • Sodium Lactate* / therapeutic use
  • Syndecan-1 / analysis
  • Syndecan-1 / blood
  • Tumor Necrosis Factor-alpha / analysis
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Endothelial Growth Factors
  • Hypertonic Solutions
  • IL10 protein, human
  • Interleukin-10
  • Interleukin-1beta
  • SDC1 protein, human
  • Sodium Lactate
  • Syndecan-1
  • Tumor Necrosis Factor-alpha