Effects of inhibitors of some mediators on the paw-edema induced by acetyl glyceryl ether phosphorylcholine in rats.

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Abstract
The characterization of acetyl glyceryl ether phosphorylcholine (AGEPC)-induced paw edema in rats was explored. Edema formation was maximum at 45 min after the injection of AGEPC. The dose for maximal response was l .mu.g/site, while edema was suppressed at higher doses. The systemic administration (s.c.) of cyproheptadine (CH, 10 mg/kg) did not inhibit this edema differently from serotonin-induced edema, while the local treatment of CH suppressed AGEPC-induced edema in a dose-dependent manner. The combination of local treatments with pyrilamine and methysergide also suppressed this edema. The s.c. injection of indomethacin (IM, 10 mg/kg) did not inhibit AGEPC edema differently from carrageenin-induced edema, while locally given IM suppressed it partially. The local treatment with caffeic acid and esculetin, lipoxygenase inhibitors, or with FPL 55712, an antagonist of SRS-A, suppressed AGEPC edema slightly. Various combinations of local treatment with IM and lipoxygenase inhibitors gave synergistic suppression of this edema. Dexamethasone strongly suppressed AGEPC edema when given both systemically and locally 3 hr before the injection of AGEPC. However, phospholipase A2 (PLA2) inhibitors, i.e. mepacrine, p-bromophenacyl bromide, chlorpromazine and tetracaine did not show the same effect as dexamethasone. These results suggest that the edema formation induced by AGEPC may involve not only the combined action of histamine and serotonin but also the synergistic action of cyclooxygenase and lipoxygenase products. Dexamethasone may inhibit this edema by mechanisms other than the inhibitory action of PLA2.