Endothelial glycocalyx of equine intestinal vessels: electron microscopic and immunohistochemical imaging.

LPS-induced endotoxemia disrupts the equine intestinal endothelial glycocalyx, potentially worsening vascular dysfunction in colic cases.

This study represents the first visualization of the endothelial glycocalyx in equine intestinal vessels, using transmission electron microscopy (TEM) and immunohistochemistry (IHC) in a controlled experimental model of endotoxemia. Six healthy horses underwent jejunal tissue collection via perfusion fixation with lanthanum nitrate at baseline and 120 minutes following IV administration of 30 ng·kg⁻¹ Escherichia coli lipopolysaccharide (LPS). TEM successfully visualized the glycocalyx ultrastructure in three of six horses, revealing morphological variability including glycocalyx thickness up to 2.5 µm and structural disruptions associated with endotoxemia. IHC panels targeting heparan sulfate, syndecan-1, catalase, and superoxide dismutase-2 (SOD-2) demonstrated endothelial reactivity only for heparan sulfate and catalase, confirming their roles as glycocalyx components in horses. Syndecan-1 and SOD-2 antibodies yielded no assessable immunoreactivity, possibly reflecting species-specific antigen limitations. LPS-induced endotoxemia appeared to cause glycocalyx structural disintegrity and shedding, with implications for vascular permeability and inflammatory cascades. These findings are clinically relevant given the high prevalence of endotoxemia in equine gastrointestinal disease, particularly colic and colitis. Limitations include small sample size, partial TEM success rate, and technical challenges inherent to glycocalyx preservation and visualization. This foundational work advances understanding of vascular pathophysiology in endotoxemic horses and supports further investigation into glycocalyx-targeted therapeutic strategies.

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