Gastrointestinal derived factors are potential triggers for the development of acute equine laminitis

Equine laminitis is the painful and debilitating condition resulting from cellular damage and inflammation of the tissues comprising the bonds supporting the pedal bone within the hoof capsule. One of the reasons why this condition is so complicated and enigmatic is its association with gastrointestinal disturbances, particularly a diet of lush grass at certain times of the year. Determining the link between disturbances to the hindgut flora and pathophysiology in the foot is one of the keys to preventing this condition. Therefore, one of the biggest challenges in equine laminitis research is to determine those events that precede the onset of the classical clinical signs of lameness, bounding digital pulses, and warm feet. A main theory for the pathogenesis of acute laminitis involves the development of vasoconstriction within the foot, which leads to ischemic and/or inflammatory tissue damage. Serotonin is an important constrictor mediator controlling digital blood flow. Certain equine hindgut bacteria produce amino acid decarboxylase enzymes that convert free amino acids into monoamines. Therefore, amines formed and released from the gastrointestinal tract are hypothesized to act as the link between the ingestion of lush grass and the digital ischemia thought to precede laminitis. Equine cecal contents contain a range of amines that are present in micromolar concentrations. Tryptamine is the most potent cecum-derived amine, causing vasoconstriction in vitro and in vivo through direct activation of serotonin receptors and displacing serotonin from platelets. Monoamines found in the cecum of the horse could potentially induce hemodynamic disturbances in the digit that result in laminar ischaemia, and so trigger laminitis.