There are no experimentally validated pharmacological means of preventing laminitis; however, locally acting pharmaceutical agents with the potential to prevent laminitis have been identified. Demonstrating therapeutic drug concentrations in lamellar tissue is essential for evaluating the efficacy of these agents. The aim of this study was to develop an experimental technique for repeatedly sampling lamellar interstitial fluid. A technique for placing ultrafiltration probes was developed in vitro using 15 cadaver limbs.
Hyperinsulinemia leads to insulin resistance of blood vessels and interferes with circulation of laminae of the equine foot. The objective of the study was to compare the digital vessel responses of clinically healthy and laminitic horses with and without experimental induction of insulin resistance. Vessel segments (artery and vein) collected after euthanasia were cut into 3-mm wide rings and were prepared in tissue baths containing Tyrode solution for response studies. Two rings of each vessel type from each horse were used as nonresistant, and two were made insulin resistant.
Objective—To investigate effects of endotoxin on leukocyte activation and infiltration of the laminar tissue in isolated perfused equine limbs.
Sample—10 right forelimbs and 3 left forelimbs collected from 10 healthy adult horses after slaughter at a licensed abattoir.
Reasons for performing study
Prophylactic digital hypothermia reduces the severity of acute laminitis experimentally but there is no evidence for its efficacy as a treatment once lameness has already developed.
To investigate the therapeutic effects of digital hypothermia, applied after the onset of lameness, in an experimental acute laminitis model.
Randomised, controlled (within subject), blinded, experimental trial.
Objective—To determine cellular changes associated with secondary epidermal laminae (SEL) in forefeet and hind feet of ponies with insulin-induced laminitis. Animals—8 ponies. Procedures—Laminitis was induced in 4 ponies by IV administration of insulin and glucose; 4 control ponies received saline (0.9% NaCl) solution IV. Laminar tissue samples obtained from the dorsal aspects of the hooves were histologically evaluated. Primary epidermal lamina (PEL) length and width and SEL length, width, and angle were determined.
Reasons for performing study
Hypoxia-inducible factor-1α (HIF-1A) is an important protein in the regulation/induction of many genes in the cellular and tissue response to hypoxia and a central mediator in inflammatory signalling. As both hypoxia and inflammatory events are purported to occur in the lamellar epidermis in sepsis-related laminitis in the equid, HIF-1A may play a central role in this disease process.
Objective—To evaluate the usefulness of Doppler ultrasonography as a method to assess changes in digital vascular dynamics in horses with systemic inflammatory response syndrome (SIRS) or laminitis.
Animals—42 adult Andalusian horses.
Laminitis is a highly debilitating disease of the foot known to have a complex and multifactorial aetiology of metabolic, inflammatory, traumatic or vascular origin. The disease has major welfare implications due to unrelenting pain associated with degenerative changes, which often necessitate euthanasia on welfare grounds. Despite this, there have been few high-quality studies investigating risk factors for equine laminitis, and only a limited number of risk factors have been previously investigated.
Radiographic studies are an essential component in evaluation of horses with laminitis. The standard radiographs that should be obtained to aid assessment of horses with laminitis are the lateromedial, horizontal dorsopalmar and dorsal 45° proximal palmarodistal oblique views. This article will summarise the assessment of these 3 projections in the laminitic horse as well as discuss the prognostic significance of common radiological abnormalities in horses with laminitis.
Although glucocorticoids have been used successfully for the treatment of noninfectious inflammatory diseases of horses for more than 35 years, their use has been attended by a fear of the induction of laminitis. This paper reviews the evidence for this fear and the possible mechanisms whereby glucocorticoids could participate in laminitis induction.