The effect of continuous digital hypothermia on lamellar energy metabolism and perfusion during laminitis development in two experimental models.
Authors: Stokes Simon M, Bertin Francois-Rene, Stefanovski Darko, Poulsen Lea, Belknap James K, Medina-Torres Carlos E, Pollitt Christopher C, van Eps Andrew W
Journal: Equine veterinary journal
Summary
# Editorial Summary: Digital Hypothermia and Lamellar Metabolism in Laminitis Continuous digital hypothermia (CDH) is an established therapeutic intervention that prevents laminitis progression, yet the precise mechanisms protecting the lamellae remained poorly understood. Researchers analysed archived lamellar tissue samples from horses subjected to two common experimental laminitis models—euglycaemic hyperinsulinaemic clamp (EHC) and oligofructose challenge—using microdialysis to measure glucose, lactate, pyruvate and perfusion markers in cooled versus ambient-temperature forelimbs. Cooling significantly reduced lactate and pyruvate production across all groups, indicating suppressed cellular metabolism, whilst lamellar glucose availability remained unchanged and perfusion decreased only in the healthy and EHC-induced models. The findings suggest that CDH operates not through preventing metabolic collapse, but rather by selectively dampening the energy-dependent pathological processes (such as inflammatory cascades and cellular migration) that drive lamellar failure, whilst preserving sufficient metabolic activity for essential tissue homeostasis. For practitioners, these results reinforce that therapeutic cooling likely works through metabolic suppression rather than prevention of nutrient starvation, supporting its use as a frontline intervention in acute laminitis alongside conventional management, though the differing perfusion response in oligofructose-induced cases hints that endocrinopathic and systemic inflammatory models may benefit from distinct mechanistic investigations.
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Practical Takeaways
- •Digital cooling (therapeutic hypothermia) reduces metabolic activity in the laminae without starving tissues of glucose, suggesting it may selectively inhibit harmful inflammatory processes during laminitis
- •The mechanism of therapeutic cooling involves reducing tissue perfusion and energy metabolism rather than causing cellular energy failure, which has implications for the duration and intensity of cooling protocols
- •Results suggest natural endocrinopathic laminitis may differ from experimental models, warranting caution when extrapolating mechanistic findings from EHC studies to clinical laminitis cases
Key Findings
- •Continuous digital hypothermia (CDH) decreased lamellar lactate and pyruvate concentrations across all groups (P<0.001 and P<0.01 respectively) without affecting lamellar glucose concentration
- •CDH reduced lamellar tissue perfusion (measured by urea clearance) in control and EHC groups (P=0.002 and P<0.001) but not in the oligofructose model (P=0.4)
- •Lactate to pyruvate ratio decreased with CDH in healthy controls (P<0.001) but not during EHC or oligofructose laminitis induction
- •CDH prevents laminitis by limiting energy supply to pathologic cellular processes while preserving glucose homeostasis critical for lamellar survival