Corticosteroid-potentiated vascular responses of the equine digit: a possible pharmacologic basis for laminitis.

Spirally cut digital arteries and veins were mounted isotonically in organ baths containing oxygenated Krebs' Q-Henseleit solution. Twelve arterial and 12 venous preparations all contracted dose dependently when epinephrine, norepinephrine, serotonin, or histamine were added to the bathing fluid. Addition of hydrocortisone or betamethasone alone did not cause contractions in any of the tissues tested. However, when hydrocortisone or betamethasone was added to vessel strips that were partially contracted (40% to 60% maximal) by epinephrine, norepinephrine, or serotonin, each vessel strip invariably underwent an additional contraction. In venous and arterial strips, dose-response curves to epinephrine, norepinephrine, serotonin, or histamine were established in the absence and in the presence of corticosteroid. Effects of the amines, except histamine, were markedly potentiated. The degree of corticosteroid/amine potentiation was greater for epinephrine than for norepinephrine and greater in the digital vein than in the corresponding artery from the same animal. Betamethasone was more potent than hydrocortisone.