Abstract
The glycocalyx is an endothelial surface layer that is essential for maintaining microvascular homeostasis. Impaired integrity of the endothelial glycocalyx may be directly related to the development of microvascular dysfunction. To explore this hypothesis, we conducted a prospective observational study on adult patients diagnosed with sepsis. The study aimed to evaluate the degree of damage to the glycocalyx and to identify correlations between microcirculatory parameters and glycocalyx thickness based on capillary diameter. Sublingual microcirculation was examined using a handheld Cytocam-incident dark field video microscope. A sidestream dark field video microscope attached to a GlycoCheck monitor was used to determine the perfused boundary regions (PBRs) of sublingual blood vessels grouped by diameter (5–9 μm, 10–19 μm, and 20–25 μm). We identified significant damage to the glycocalyx in sublingual blood vessels of all the aforementioned diameters in septic patients compared to healthy age-matched controls. Furthermore, we found that the PBRs of the smallest capillaries (diameter class 5–9µm) correlated moderately and inversely with both total and perfused blood vessel densities. Collectively, our data suggest that there may be a functional relationship between damage to the endothelial glycocalyx of the smallest capillaries and alterations in the microcirculation observed in response to sepsis.
Highlights
The endothelial glycocalyx (EG) is a component of the luminal layer of intact blood vessels that is composed of proteoglycans and glycosaminoglycans
We identified no correlation between PBR5–9 and PBR20–25
We found no correlations between perfused boundary regions (PBRs) and mean arterial pressure (MAP), heart rate (HR), C-reactive protein (CRP), interleukin (IL-6), APACHE II scores, or Sequential Organ Failure Assessment (SOFA) scores
Summary
The endothelial glycocalyx (EG) is a component of the luminal layer of intact blood vessels that is composed of proteoglycans and glycosaminoglycans. Impaired EG integrity may lead directly to changes in vascular function, including increased permeability, altered modulation of biochemical signals, and impaired hemostasis [2] These pathophysiological responses all contribute to the pathogenesis of sepsis and associated organ failure. Shedding of the EG results in the exposure of adhesion molecules. Activation of these molecules leads to the recruitment of leukocytes and platelets and the development of intravascular thrombi, fibrin formation, vascular hyporeactivity, increased vascular permeability, and results in circulatory dysfunction [3,4]
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