Surgical delay and arachidonic acid metabolites: evidence for an inflammatory mechanism: an experimental study in rats.
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 PGF2 alpha 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 PGF2 alpha 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.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D015237:Dinoprost; D015232:Dinoprostone; D007249:Inflammation / Q000378:metabolism*; D008297:Male; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012867:Skin / Q000378:metabolism*; D013524:Surgical Flaps; D013929:Thromboxane B2 / Q000378:metabolism; D013997:Time Factors
D001095:Arachidonic Acids; D011458:Prostaglandins E; D011460:Prostaglandins F; D016718:Arachidonic Acid; D013929:Thromboxane B2; D015237:Dinoprost; D015232:Dinoprostone