ArticleJournal of veterinary internal medicine2017
Effect of Delayed Digital Hypothermia on Lamellar Inflammatory Signaling in the Oligofructose Laminitis Model.
Article in Journal of veterinary internal medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Effect of Continuous Digital Hypothermia on Lamellar Inflammatory Signaling When Applied at a Clinically-Relevant Timepoint in the Oligofructose Laminitis Model.Journal of veterinary internal medicine · 2018Trial
- Angelica polysaccharide attenuates LPS-induced inflammation response of primary dairy cow claw dermal cells via NF-κB and MAPK signaling pathways.BMC veterinary research · 2021Article
- Effect of digital hypothermia on lamellar inflammatory signaling in the euglycemic hyperinsulinemic clamp laminitis model.Journal of veterinary internal medicine · 2020Article
- Laminar Inflammation Responses in the Oligofructose Overload Induced Model of Bovine Laminitis.Frontiers in veterinary science · 2020Article
- Interleukin-17A pathway target genes are upregulated in Equus caballus supporting limb laminitis.PloS one · 2020Article
- A Comparative Review of Equine SIRS, Sepsis, and Neutrophils.Frontiers in veterinary science · 2019Review
- Whole body and partial body cryotherapies - lessons from human practice and possible application for horses.BMC veterinary research · 2018Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn the oligofructose (OF) model of sepsis-related laminitis (SRL), digital hypothermia ("cryotherapy") initiated before the onset of clinical signs is reported not only to limit lamellar injury, but also to cause marked inhibition of lamellar inflammatory signaling. HYPOTHESIS/
objectivesBecause hypothermia also has been reported to be protective when not initiated until the onset of lameness in the OF model of SRL, we hypothesized that the lamellar protection conferred by hypothermia is caused by local lamellar inhibition of inflammatory signaling as described when hypothermia was initiated earlier in the disease process. ANIMALS: Eight Standardbred geldings aged 3-11 years with no lameness and no abnormalities of the feet detectable by gross or radiographic examination.
methodsUsing the OF model of SRL, lamellar mRNA concentrations of proinflammatory cytokines, chemokines, and endothelial adhesion proteins were compared between samples from treated limbs (CRYO, submerged in ice water for 36 hour starting at the onset of lameness), untreated limbs (NON-CRYO, opposite limb from CRYO limbs maintained at ambient temperature), and untreated limbs from normal horses in which laminitis was not induced (CON).
resultsAlthough OF administration resulted in increases in lamellar mRNA concentrations of several inflammatory mediators in NON-CRYO limbs (vs CON), digital hypothermia had no significant effect on these increases. CONCLUSIONS AND CLINICAL IMPORTANCE: The lack of inflammatory inhibition in lamellar tissue samples in our study indicates that the protective effects of digital hypothermia instituted at the onset of clinical signs of laminitis do not arise from inhibition of inflammatory pathways.
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