Equine laminitis: its development coincides with increased sublamellar blood flow

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Abstract
The effect of alimentary carbohydrate overload on hoof temperature was investigated to determine the state of the sublamellar vasculature preceding the onset of equine laminitis. Hoof, core and ambient temperatures and heart rate were logged continuously in 21 mature Standardbred horses kept in an environmental chamber set at 10 degrees C. Recording hoof temperature was a successful, noninvasive, method to measure indirectly, shifts in digital blood flow against a background of cold induced, physiological, vasoconstriction. High hoof temperatures were assumed to indicate digital vasodilation and low hoof temperatures digital vasoconstriction. Seven horses were either untreated or sham treated controls. A slurry of ground wheat flour (17.5 g/kg) was administered via nasogastric tube to 13 horses all of which were humanely killed 48 h later. Histological sections of the lamellar tissues were examined for evidence of laminitis. Analysis of mean hoof temperature graphs showed that horses judged laminitis positive had experienced a period of prolonged digital vasodilation 16-40 h after carbohydrate overload. Laminitis negative horses experienced no such period of vasodilation and never had hoof temperatures significantly (except once, at 28 h) above that of controls. The only parameter which significantly differentiated the laminitis positive from laminitis negative horses, between 12 and 32 h after carbohydrate overload, was foot temperature, which was significantly higher in laminitis positive horses (P < 0.05). Therefore, a period of sublamellar vasodilation, 12 to 40 h after alimentary carbohydrate overload precedes the onset of laminitis. If the digital circulation sustains vasoconstriction during this period then laminitis does not occur. We propose that the period of increased digital blood flow in laminitis positive horses, concomitant with the severe metabolic crisis brought on by the alimentary carbohydrate overload, may expose the lamellar tissues to a concentration of blood borne factors sufficient to trigger lamellar separation.