Leukocyte emigration in the early stages of laminitis

Plasma concentrations of endotoxin and platelet activation in the developmental stage of oligofructose-induced laminitis.

Summary
Reasons for performing study: There is a need to assess the laminar inflammatory response in a laminitis model that more closely resembles clinical cases of sepsis-related laminitis than the black walnut extract (BWE) model.

Objectives: To determine if a similar pattern of laminar inflammation, characterised by proinflammatory cytokine expression, occurs in the CHO model of laminitis as has been previously reported for the BWE model.

Methods: Sixteen horses administered 17.6 g of starch (85% corn starch/15% wood flour)/kg bwt via nasogastric (NG) tube were anaesthetised either after developing a temperature >38.9°C (DEV group, n = 8) or at onset of Obel grade 1 lameness (OG1 group, n = 8). Control horses (CON group, n = 8) were anaesthetised 24 h after NG administration of 6 l of deionised water. Laminar tissue was collected from horses while under anaesthesia, followed by humane euthanasia. Real time-quantitative PCR was used to assess laminar mRNA concentrations of genes involved in inflammatory signalling.

Results: Increased mRNA concentrations (P<0.05) for IL-1β, IL-6, IL-12p35, COX-2, E-selectin and ICAM-1 were present in laminae from horses with OG1 lameness but not at the DEV time, when compared to the CON horses. No differences between the groups were found for IL-2, IL-4, IL-10, TNF-α, IFN-γ or COX-1 at either the DEV or OG1 time points.

Conclusions: There was a notable difference in the temporal pattern of inflammatory events between the BWE and CHO models, with the majority of laminar inflammatory events appearing to occur at or near the onset of lameness in the CHO model, whereas many of these events peak earlier in the developmental stages in the BWE model. This suggests that, in addition to circulating inflammatory molecules, there may be a local phenomenon in the CHO model resulting in the simultaneous onset of multiple laminar events including endothelial activation, leucocyte emigration and proinflammatory cytokine expression.

Potential relevance: The similar (although somewhat delayed) inflammatory response in the CHO model of laminitis indicates that inflammatory signalling is a consistent entity in the pathophysiology of laminitis.

Laminar inflammatory gene expression in the carbohydrate overload model of equine laminitis

Objective—To determine proinflammatory gene expression, endothelial adhesion molecule gene expression, and matrix metalloproteinase (MMP) concentrations in laminar specimens at 1.5 hours after administration of black walnut extract (BWE) and to compare these values with later time points. Animals—25 horses. Procedures—After nasogastric administration of BWE, anesthesia was induced at 1.5 hours in early time point (ETP) horses (n = 5), between 3 and 4 hours in developmental time point horses (5), and between 9 and 10 hours in acute onset of lameness time point horses (5). Anesthesia was induced at 3 and 10 hours after nasogastric administration of water in 2 groups of control horses (3-hour control group, n = 5; 10-hour control group, 5). Real-time quantitative PCR assay was performed on laminar specimens from control and ETP horses for cyclooxygenase (COX)-1, COX-2, interleukin (IL)-1β, tumor necrosis factor-α, IL-6, IL-8, IL-10, MMP-2, and MMP-9 gene expression; and on laminar specimens from all groups f...

Early laminar events involving endothelial activation in horses with black walnut– induced laminitis

Background:Recent reports indicate increased amounts of mRNA from inflammation-related genes in the prodromal stage of laminitis.

Hypothesis:Cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) undergo distinct patterns of expression in equine laminae in the developmental stage (DEV) and acute clinical stage (LAM) of laminitis.

Animals:Horses selected from an outbred population were placed into 1 of 4 groups: DEV (n = 5), CON-3h (control group for DEV, n = 5), LAM (n = 5) and CON-10h (control group for LAM, n = 5).

Methods:Laminar and skin samples were obtained from (1) animals either undergoing leukopenia (DEV) or the onset of clinical signs of laminitis (LAM) after black walnut extract (BWE) administration and (2) animals either 3 (CON-3h) or 10 (CON-10h) hours after administration of water. Real-time quantitative polymerase chain reaction (RT-qPCR), immunoblotting, and immunohistochemical analysis were performed for COX-1 and COX-2.

Results:Upon immunohistochemical analysis of all 4 groups, COX-2 was expressed by most viable epithelial cells in both laminae and skin. COX-1 exhibited similar epithelial expression to COX-2 in skin epidermis, but was expressed exclusively in the basal layer of laminar epidermis. COX-1 protein was not detectable in dermal vasculature of equine skin or laminae, whereas COX-2 was present in endothelial and vascular smooth muscle cells of dermal vasculature in both skin and laminae in all groups. A marked increase in laminar COX-2 protein concentrations was detected on immunoblotting in the DEV group, although a lesser increase was observed in the LAM group.

Conclusions and Clinical Importance: COX-2 protein expression is markedly increased in the resident laminar cell types in the developmental stage of BWE-induced laminitis.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1939-1676.2006.tb00721.x

Cyclooxygenase expression in the early stages of equine laminitis: a cytologic study.

Objective—To compare the levels of mRNA expression of cycooxygenase (COX)-1 and COX-2 in the digital laminae of normal horses and horses in the developmental stages of laminitis experimentally induced by administration of black walnut extract (BWE). Sample Population—Samples of mRNA extracted from the digital laminae of 5 control horses and 5 horses at the onset of leukopenia after administration of BWE. Procedure—Specimens of laminae were collected from anesthetized horses prior to euthanasia. Expression of COX-1 and COX-2 mRNA in laminae of control and affected horses was evaluated via realtime quantitative polymerase chain reaction techniques. Results—Expression of COX-2 mRNA was significantly increased in the BWE-treated group, compared with that in control horses. In contrast to COX-2 regulation, COX-1 mRNA expression was not significantly different between groups. Interestingly, despite consistent clinical signs such as leukopenia in all BWE-treated horses, distinct differences in COX-2 mRNA expression were detected among those 5 horses (compared with values for control horses, the increase in COX-2 mRNA expression ranged from no increase to a 30-fold increase). Conclusions and Clinical Relevance—Results indicated that there was a significant upregulation of COX2 mRNA expression during the developmental stages of laminitis, with no significant change in expression of the COX-1 isoform. These data appear to provide support for aggressive use of nonsteroidal anti-inflammatory drugs in horses at risk for laminitis; further investigation into the clinical value of selective COX-2 inhibitors for treatment of laminitis in horses appears to be warranted. (Am J Vet Res 2004;65:1724–1729)

Expression of the cyclooxygenase isoforms in the prodromal stage of black walnut-induced laminitis in horses.

Navicular syndrome is a chronic and often progressive disease affecting the navicular bone and bursa, deep digital flexor tendon (DDFT), and associated soft tissue structures composing the navicular apparatus. This syndrome has long been considered one of the most common causes of forelimb lameness in horses. Diagnosis of navicular syndrome is based on history, physical examination, lameness examination, and peripheral and/or intraarticular diagnostic anesthesia. Several imaging techniques (e.g., radiography, ultrasonography, nuclear scintigraphy, thermography, computed tomography [CT], magnetic resonance imaging [MRI]) are used to identify pathologic alterations associated with navicular syndrome. Radiographic changes of the navicular bone are not pathognomonic for navicular syndrome. Additionally, not all horses with clinical signs of navicular syndrome have radiographic changes associated with the navicular bone. Therefore, newer imaging modalities, including CT and especially MRI, can play an important role in identifying lesions that were not observed on radiographs. Navicular bursoscopy may be necessary if the clinical findings suggest that lameness originates from the navicular region of the foot and if other imaging modalities are nondiagnostic. With new diagnostic imaging techniques, clinicians are learning that anatomic structures other than the navicular bursa, navicular bone, and DDFT may play an important role in navicular syndrome.

/pdf/navicular-syndrome-in-equine-patients-anatomy-causes-and-3bzw5mu6vi.pdf

Navicular Syndrome in Equine Patients: Anatomy, Causes, and Diagnosis*

Navicular syndrome is a chronic, progressive condition affecting the navicular bone and bursa, deep digital flexor tendon (DDFT), and associated soft tissue structures composing the navicular apparatus. The treatment options for navicular syndrome are as varied as the proposed causes of the condition. The severity of clinical signs, intended use and workload of the horse, and owner compliance with therapy are important considerations in developing a treatment plan. Nonsurgical treatment of navicular syndrome consists of rest, hoof balance and corrective trimming/shoeing, and medical therapy, including administration of systemic antiinflammatories, hemorheologic medications, and intraarticular medications. While surgical therapy can include desmotomy of the collateral (suspensory) ligaments of the navicular bone, palmar digital neurectomy is more commonly performed when medical therapy is ineffective. Recently, adjunct therapies, such as acupuncture and extracorporeal shock wave therapy, have also been used to treat horses with navicular syndrome. Because of the wide range of pathologic changes and the lack of a definitive cure associated with navicular syndrome, treatment is directed toward the individual horse, focusing on the management of clinical signs to alleviate stress and retard degenerative changes of the navicular bursal and navicular regions.

Treating navicular syndrome in equine patients.

Effect of PO Administered Gabapentin on Chronic Lameness in Horses

Objective: To develop a tenoscopic approach for desmotomy of the accessory ligament of the deep digital flexor tendon (AL-DDFT) in horses.



Study Design: Experimental.



Animals: Cadaveric forelimbs (n=10) and 4 forelimbs from 2 horses anesthetized for terminal teaching procedures, and 12 forelimbs of 6 experimental horses.



Methods: Saline distention of the carpal flexor sheath facilitated insertion of an arthroscope into the distal medial aspect of the sheath between the AL-DDFT and deep digital flexor tendon (DDFT). Location of an instrument portal on the lateral aspect of the metacarpus was identified with a needle. The lateral aspect of the AL-DDFT was transected and the arthroscope and instrument were switched to transect the remaining fibers on the medial aspect. Cadaveric specimens were dissected for evaluation. Experimental horses were monitored for 30 days postoperatively.



Results: Minor complications including incomplete division of the AL-DDFT and shallow incision into the suspensory ligament were observed in some cadaver specimens. The AL-DDFT was completely transected in all experimental horses with no suspensory ligament damage. Mean±SD surgical time (incision to skin closure) was 28.3±11.8 minutes. On ultrasonographic examination, transection of the AL-DDFT was complete in all experimental horses. Minor DDFT fiber disruption was noted in 1 limb during ultrasound examination at day 30.



Conclusions: A tenoscopic approach through the carpal flexor sheath provided adequate access for desmotomy of the AL-DDFT.

Evaluation of a tenoscopic approach for desmotomy of the accessory ligament of the deep digital flexor tendon in horses.

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

R. Wayne Waguespack

Author Tools

Chat about Author