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Effects of amide local anaesthetics on eicosanoid formation in burned skin
Author(s) -
Jönsson A.,
Cassuto J.,
Tarnow P.,
Sinclair R.,
Bennett A.,
Tavares I. A.
Publication year - 1999
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1034/j.1399-6576.1999.430605.x
Subject(s) - medicine , prilocaine , lidocaine , saline , eicosanoid , anesthesia , pathophysiology , prostaglandin , pharmacology , radioimmunoassay , biochemistry , chemistry , arachidonic acid , enzyme
Bacground: Previous studies have demonstrated potent inhibition of burn oedema and progressive ischaemia by local anaesthetics. Since eicosanoids have been suggested to play an important role in the pathophysiology of burns, we compared in the present ex vivo study the effects of topical lidocaine/prilocaine cream (EMLA ® , ASTRA, Sweden) and intravenous lidocaine with that of saline on eicosanoid formation by normal and burned rat skin. Methods: A full‐thickness burn trauma was induced in the abdominal skin. All the agents were given 5 min postburn until 2 h after the trauma. The experimental skin was subsequently removed and incubated in Krebs solution for 1 h. Eicosanoid concentrations in the solution were analysed by radioimmunoassay. Results: EMLA ® cream induced a significant inhibition of TXB 2 ( P <0.05) and 6‐Keto‐PGF 1α ( P <0.01) but not of PGE release from burned skin as compared to saline treatment. Intravenous lidocaine infusions did not significantly influence the release of any of the measured eicosanoids versus saline. Conclusion: In conclusion, the lack of effect of intravenous lidocaine could relate to the severe burn trauma inducing rapid ischaemia which may have interfered with the delivery of the agent to the burned tissues or to insufficient concentrations achieved in the burn area. Topical treatment of burned skin with a local anaesthetic cream significantly reduced the release of TXB 2 and 6‐Keto‐PGF 1α , suggesting a possible mechanism of action in progressive burn ischaemia.