Open AccessRole of Oxidative Tissue Injury in the Pathophysiology of Experimentally Induced Equine Laminitis: A Comparison of 2 Models
Author(s) -
Burns T.A.,
Westerman T.,
Nuovo G.J.,
Watts M.R.,
Pettigrew A.,
Yin C.,
Belknap J.K.
Publication year - 2011
Publication title -
journal of veterinary internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.356
H-Index - 103
eISSN - 1939-1676
pISSN - 0891-6640
DOI - 10.1111/j.1939-1676.2011.0706.x
Subject(s) - laminitis , medicine , pathophysiology , oxidative phosphorylation , pathology , horse , biochemistry , paleontology , biology , chemistry
Background: Oxidative stress reportedly plays a role in sepsis‐induced organ dysfunction and failure in many species. In septic horses, laminae are targeted; evidence of laminar oxidative stress has been reported experimentally in the black walnut extract (BWE) model. Carbohydrate (CHO)‐induced laminitis may be more similar to clinical sepsis‐related laminitis than the BWE model in that animals with CHO‐induced disease commonly develop laminar failure. The role of oxidative stress in the CHO model remains unknown. Hypothesis/Objectives: Markers of oxidative stress will be increased in laminae from horses with BWE‐ and CHO‐induced laminitis. Animals: Banked laminar tissue from various time points from animals subjected to BWE (n = 15) and CHO (n = 20) protocols. Methods: Laminar 4‐hydroxynonenal (4‐HNE) and protein carbonyl content were evaluated by slot blot analysis. Laminar 3‐nitrotyrosine (3‐NT) immunohistochemistry was performed. Results: The number of laminar 3‐NT (+) cells was increased at developmental and Obel grade 1 (OG1) time points in the BWE model (versus control [CON]; P = .013) and lower in OG1 tissues than CON in the CHO model ( P = .04). No change in 4‐HNE content was observed in the CHO model, and no increase in laminar protein carbonyl content was present in either model ( P > .05). Conclusions and Clinical Importance: These results do not support a prominent role for oxidative stress at examined time points in CHO‐overload laminitis and support transient oxidative stress in the BWE model. Tissue oxidation does not appear to be a central early pathophysiologic event in CHO‐associated laminitis.