Abstract
In a rat skin flap model, surgical delay produced an increase in the production of arachidonic acid metabolites, with a derangement of the normal equilibrium between PGE2 and PGF2α and a marked increase in the vasoconstrictive substance, thromboxane. During the delay period, there is a gradual decrease in tissue levels toward normal. Subsequent elevation of the delayed flap produces a blunted response in thromboxane production, an increase in PGE2 levels and increased flap survival. Acute elevation of an undelayed flap produced more marked elevation of all metabolites, with prolonged elevation of the vasoconstrictive PGF2α and thromboxane, progressive ischemia and decreased flap survival. A key role in inflammation, mediated by these inflammatory mediators, is postulated in the mechanism of delay.
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