Effect of acute sublethal endotoxaemia on in vitro digital vascular reactivity in horses.
Authors: Zerpa, Vega, Vasquez, Ascanio, Campos, Sogbe, Romero, Ascanio, García
Journal: Journal of veterinary medicine. A, Physiology, pathology, clinical medicine
Summary
# Editorial Summary: Acute Endotoxaemia and Digital Vascular Dysfunction in Horses Endotoxaemia is implicated in laminitis pathogenesis, yet the precise vascular mechanisms remain poorly understood. Zerpa and colleagues induced acute sublethal endotoxaemia in 11 healthy horses using intravenous lipopolysaccharide (0.25 µg/kg), then examined contractile and relaxation responses of isolated palmar digital arteries and veins harvested three hours post-endotoxin challenge. The endotoxaemic horses developed expected systemic signs including colic, diarrhoea, tachycardia and leucopenia; critically, their digital arteries demonstrated heightened sensitivity to the vasoconstrictor phenylephrine (leftward shift in concentration-response curve) whilst endothelium-dependent relaxation to acetylcholine was significantly impaired in both arteries and veins. These vascular changes—increased vasoconstriction coupled with reduced endothelial vasodilatory capacity—suggest that acute endotoxaemia creates a prothrombotic digital vascular environment characterised by sustained constriction and diminished compensatory relaxation, mechanisms that may precipitate the digital ischaemia underlying laminitis. For practitioners, this work underscores why aggressive systemic endotoxin management during colic, colitis or septic conditions represents critical laminitis prophylaxis, as even subclinical endotoxaemic exposure may compromise digital vascular homeostasis before overt lameness develops.
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Practical Takeaways
- •Horses with acute endotoxaemia show altered digital vascular reactivity that may contribute to laminitis development through reduced blood flow and prothrombotic mechanisms
- •Digital endothelial dysfunction during the acute phase of endotoxaemia represents a potential therapeutic target to prevent or mitigate laminitis progression
- •The vascular changes occur rapidly (within 3 hours) and persist despite absence of histopathological changes, suggesting functional rather than structural vascular damage in early endotoxaemia
Key Findings
- •Acute sublethal endotoxaemia caused a leftward shift in concentration-response curves to phenylephrine in digital artery rings, indicating increased arterial reactivity
- •Acetylcholine-induced endothelium-dependent vasodilation was significantly reduced in both arteries and veins after endotoxaemia
- •Response to sodium nitroprusside and depolarizing Krebs solution remained unchanged, suggesting preserved smooth muscle function
- •Impaired digital endothelial function during acute endotoxaemia may predispose to prothrombotic state and reduced vasodilatory capacity