Corticosteroid-potentiated vascular responses of the equine digit: a possible pharmacologic basis for laminitis.
Authors: Eyre, Elmes, Strickland
Journal: American journal of veterinary research
Summary
# Editorial Summary This 1979 investigation examined how corticosteroids affect blood vessel reactivity in equine digits, using isolated arterial and venous tissue strips from the distal limb mounted in organ baths and challenged with various vasoactive substances. Whilst corticosteroids alone produced no direct contraction, hydrocortisone and betamethasone significantly amplified the contractile response of digital vessels to catecholamines (epinephrine and norepinephrine) and serotonin, with betamethasone demonstrating greater potency and the effect being more pronounced in digital veins than arteries. The degree of potentiation correlated with dose and was notably stronger for epinephrine than norepinephrine, suggesting a pharmacologic mechanism by which systemically administered corticosteroids could exacerbate vasoconstriction in an already compromised digital circulation. These findings provide experimental evidence for a long-suspected link between corticosteroid administration and laminitis risk, proposing that corticosteroids do not independently damage the laminar blood supply but rather render already-sensitised vessels hyperresponsive to endogenous vasoconstrictors. For practitioners, this work underpins the cautionary approach toward corticosteroid use in horses with predisposing laminitis risk factors or acute systemic disease, as even therapeutic doses may dangerously amplify vasoconstriction in the digit.
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Practical Takeaways
- •Corticosteroid use in horses may increase digital vasoconstriction when circulating catecholamines are elevated (stress, pain, exercise), potentially impairing digital blood flow and contributing to laminitis risk
- •Betamethasone poses greater laminitis risk than hydrocortisone based on its superior potentiation of vasoconstrictive responses in digital vessels
- •Clinical vigilance is warranted when administering corticosteroids to horses, particularly those at risk for laminitis or experiencing stress-induced catecholamine release
Key Findings
- •Corticosteroids (hydrocortisone and betamethasone) alone did not cause vessel contractions but potentiated contractions induced by epinephrine, norepinephrine, and serotonin in equine digital arteries and veins
- •Potentiation effect was greater for epinephrine than norepinephrine and more pronounced in digital veins than arteries
- •Betamethasone demonstrated greater potentiating potency than hydrocortisone across all tested vasoconstrictive agents
- •Corticosteroid-potentiated vascular responses may represent a pharmacologic mechanism underlying laminitis pathogenesis