Abstract

Lidocaine (100mg 2%) injected into the carpal joint was used to evaluate the inflammatory response induced by injection (1.5ng) of intra-articular E. coli lipopolysaccharide (LPS) endotoxin. Seventeen male Mangalarga horses aged two to three years were divided into three groups and in all animals was injected 0.9% saline (SAL) in the left carpus (LC), and in the right carpus (RC) one of the following combinations were injected: group A (n=6) LPS plus SAL; group B (n=6) LPS plus lidocaine; group C (n=5) lidocaine plus SAL. Synovial fluid and blood samples were collected immediately before the injection of LPS (T0), and at 1.5 (T1), 3 (T2), 6 (T3), 12 (T4) and 36 hours (T5) after the injection. Clinical and physical variables and cellular and biochemical characteristics of the synovial fluid were evaluated at the same time. The local and systemic inflammatory response was evaluated by measurement of mean serum and synovial fluid TNF-alpha concentration. A rise in TNF-alpha concentration in LPS injected joints at 3h in group A and from 1.5h to 3h in group B was observed. It is concluded that LPS triggered an inflammatory process and that lidocaine did not inhibit or attenuate the LPS-induced synovitis nor the synthesis and release of TNF-alpha .

Highlights

  • Musculoskeletal injuries involving distal limb joints remain the greatest cause of loss of athletic performance in racehorses industry (Todhunter and Lust, 1992)

  • Interleukin-1 (IL-1) and tumor necrosis factor (TNF) have been documented to contribute to joint destruction by induction of degrading proteases and by inducing synovial cells, synovial fibroblasts, and chondrocytes to secrete prostaglandin E2 (Dayer et al, 1985; Campbell et al, 1990); these cytokines have been associated with synovitis induced by endotoxin in horses (Price et al, 1992; Hawkins et al, 1993)

  • During the initial phase of synovitis induced by intraarticular administration of endotoxin in horses, TNF was one of the first cytokines secreted into the joint fluid (Hawkins et al, 1993)

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Summary

Introduction

Musculoskeletal injuries involving distal limb joints remain the greatest cause of loss of athletic performance in racehorses industry (Todhunter and Lust, 1992). The interaction between the synovium and articular cartilage is complex, in vitro and in vivo evidence suggests that structural and functional alterations in the articular tissues intimately affect the other tissues of the joint (Snyderman, 1986). These studies indicate that release of proteases with degrading activities is responsible for damaging the articular cartilage (Saklatvala, 1986). The secretion of these proteases is induced by several cytokines produced locally by macrophages and synovial cells (Dayer et al, 1985; Campbell et al, 1990). During the initial phase of synovitis induced by intraarticular administration of endotoxin in horses, TNF was one of the first cytokines secreted into the joint fluid (Hawkins et al, 1993)

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