2001
DOI: 10.1016/s0305-4179(00)00077-2
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A new technique for the analysis of endogenous mediators released following thermal injury

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Cited by 11 publications
(6 citation statements)
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References 28 publications
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“…A significant inhibition of PGF 2α release into the circulation was seen during systemic administration of lidocaine in dogs with cardiac arrhythmias (70). In a recent study using a technique allowing for the in vivo analysis of inflammatory mediators released post‐burn (71), a potent inhibition of PGE 1 and PGE 2 release was demonstrated when treating the burned skin in the intact animal with a topical local anesthetic cream (71), thus confirming an earlier report showing reduced PGE release from isolated pieces of gastric mucosa by lidocaine (67) (Fig. 3).…”
Section: Effects Of Local Anesthetics On Synthesis and Release Of Infsupporting
confidence: 76%
“…A significant inhibition of PGF 2α release into the circulation was seen during systemic administration of lidocaine in dogs with cardiac arrhythmias (70). In a recent study using a technique allowing for the in vivo analysis of inflammatory mediators released post‐burn (71), a potent inhibition of PGE 1 and PGE 2 release was demonstrated when treating the burned skin in the intact animal with a topical local anesthetic cream (71), thus confirming an earlier report showing reduced PGE release from isolated pieces of gastric mucosa by lidocaine (67) (Fig. 3).…”
Section: Effects Of Local Anesthetics On Synthesis and Release Of Infsupporting
confidence: 76%
“…Lidocaine administration significantly secret IL-8 and IL-10 in cell culture experiments and this effect can mediate inhibition of NFkb via decrease IkB phosphorylation (Lang et al, 2009). In a recent study a potent inhibition of PGE 1 and PGE 2 release was demonstrated when treating the burned skin in the intact animal with a topical local anesthetic cream (Yregård et al, 2001), thus confirming an earlier report showing reduced PGE 2 release from isolated pieces of gastric mucosa by lidocaine (Goel et al, 1994). These inhibitory effects on PGE 2 , known to play a significant role in the mechanisms responsible for inflammatory pain, could account for some of the potent analgesic effects of intravenous lidocaine reported in burn patients (Jönsson et al, 1999, Cassuto andTarnow, 2003) and in patients having undergone surgery (Cassuto et al, 1995;Chen et al, 2013).…”
Section: Discussionmentioning
confidence: 99%
“…In mammals, axon degeneration is known to produce post-burn neuropathic-like pain (Fauerbach et al, 2005; Schneider et al, 2006; Wong and Turner, 2010), and expression of pro-inflammatory cytokines that induce an inflammatory response in the organism (Summer et al, 2008). In addition, these burn effects will probably induce macrophage activation and migration to the site of injury (Yregård et al, 2001; Shields et al, 2012; Rosenberg et al, 2012). Inflammation and neuropathic pain have been shown to activate a list of factors in key neuromodulatory regions in mammals, like dorsal root ganglia, spinal cord neurons and neurons of the brain.…”
Section: Discussionmentioning
confidence: 99%
“…Animal in vivo experimentation, above all in the field of pain and nociception, presents ethical and scientific limitations. Rats and mice are considered the most useful animal models in this context, being suitable for genetic manipulation and having a large choice of mutants already available (Nozaki-Taguchi and Yaksh, 1998; Yregård et al, 2001; Wang et al 2005; Mogil and Basbaum, 2011; Shields et al, 2012). Studies of skin burns in animal models showed how axons innervating the tissue could be severely affected either in the short-term period directly by the burns (deCamara et al, 1982; Summer et al, 2007), or by the scar tissue, that can heavily affect axons growth in the long-term (Summer et al, 2007; Morellini et al, 2012).…”
Section: Introductionmentioning
confidence: 99%