The effect of continuous digital hypothermia on lamellar energy metabolism and perfusion during laminitis development in two experimental models.

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Continuous digital hypothermia (CDH) prevents lamellar failure in the euglycaemic hyperinsulinaemic clamp (EHC) and oligofructose (OF) laminitis models, but the mechanisms remain unclear. To evaluate the effects of CDH on lamellar energy metabolism and perfusion in healthy horses and during EHC and OF laminitis models. In vivo experiment. Archived samples were used from Standardbred geldings that received no treatment (CON) (n=8) or underwent EHC (n=8) or OF (n=6) laminitis models. Both forelimbs were instrumented with a lamellar microdialysis system, and one forelimb was cooled (CDH) with the other maintained at ambient temperature (AMB). Microdialysate was collected every 6hours and analysed for glucose, lactate and pyruvate concentrations and lactate to pyruvate ratio (L:P). Microdialysis urea clearance was used to estimate lamellar tissue perfusion. Data were analysed using a mixed-effects linear regression model. Glucose did not change in CDH limbs relative to AMB in CON (P=.3), EHC (P=.3) or OF (P=.6) groups. There was a decrease in lactate (P<.001) and pyruvate (P<.01) in CDH limbs relative to AMB in all groups. L:P decreased in CON CDH relative to CON AMB (P<.001) but was not different in EHC (P=.6) and OF (P=.07) groups. Urea clearance decreased in CDH limbs relative to AMB in CON (P=.002) and EHC (P<.001), but not in OF (P=.4). The EHC model may not mimic natural endocrinopathic laminitis. CDH caused a marked decrease in lamellar glucose metabolism (CON, EHC and OF) and perfusion (CON and EHC) without affecting lamellar glucose concentration. Although cellular energy failure is not a primary pathophysiological event in EHC and OF laminitis models, CDH may act by limiting energy supply to pathologic cellular processes whilst preserving those critical to lamellar homoeostasis.