A simple technique for preoperative teaching and planning.
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Humans↗
Biomedical subjects
S Shatkin
Publications and source records attributed to S Shatkin.
Arachidonic acid metabolites: basic concepts relevant to plastic surgery.
AA is the precursor of oxygenated metabolites called the eicosanoids, that are generated by the cyclooxygenase, lipoxygenase, or cytochrome P450 enzymatic pathways. The biologically active eicosanoids are labile, usually but not always, act near their site of synthesis, and are not stored in any tissue to any appreciable degree. In most tissues, there is a continuous low-level synthesis that is probably essential to normal function. Injury or surgical trauma can evoke a dramatic change in the quality and quantity of the metabolites. Pharmacologic manipulation of the pathways of AA metabolism, or alteration of the effects of AA metabolites, can significantly improve tissue perfusion in a variety of clinical situations. (See Figure 1 for a schematic summary of the pathways involved in arachidonic acid metabolites.
Animals↗
Modulation of arteriolar blood flow by inhibitors of arachidonic acid oxidation after thermal injury: possible role for a novel class of vasodilator metabolites.
To examine the contribution of arachidonic acid (AA) metabolites to the maintenance of cutaneous vasomotor tone after thermal injury, enzyme inhibitors were topically applied to the hamster cheek pouch before and after a spot burn. By use of video microscopy, blood flow was measured in adjacent arterioles that supplied the injured site. Ringer's solutions containing no drug (vehicle), indomethacin (cyclooxygenase inhibitor), BW755c (cyclooxygenase/lipoxygenase inhibitor), or ketoconazole (lipoxygenase/cytochrome P450 inhibitor) continuously suffused the entire tissue. There were no effects of these drugs on preburn blood flow at concentrations that blocked the vascular effects evoked by topical AA. In all groups, blood flow transiently increased after burn and thereafter decreased to levels that were altered by treatment. These results could not be attributed to alterations in vascular reactivity because neither the burn nor the drugs altered the vasodilation evoked by adenosine or prostacyclin. Relative to Ringer's, indomethacin had no effect, BW755c caused vasodilation, and ketoconazole caused vasoconstriction, which suggests that cytochrome P450 products might be vasoactive mediators in injured tissue. Therefore, purified synthetic compounds were compared with known vasodilators. The potency was prostacyclin greater than 12R-hydroxyeicostetraenoic acid greater than adenosine = 5,6 epoxyeicosatrienoic acid greater than AA, which supports the hypothesis that AA can be the source of a novel class of nonprostaglandin vasodilator compounds. In addition, at least one of the vasodilator responses was stereospecific. Nevertheless, the exact explanation for the differential effects of AA inhibitors on postburn blood flow is unknown.
4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
The deltoscapular flap.
We present a young patient in whom a large soft tissue defect of the neck was repaired with a deltoscapular flap.
Adolescent↗