English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

Background  In 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/Objectives  Because 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.    Methods  Using 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 ).    Results  Although  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.

Effect of Delayed Digital Hypothermia on Lamellar Inflammatory Signaling in the Oligofructose Laminitis Model