The source of thromboxane and prostaglandins in experimental inflammation

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Abstract
1 Although cyclo-oxygenase products have been detected at inflammatory sites the tissue of origin remains uncertain. 2 Inflammatory exudates were collected from rats 4, 6, 8, 12 or 24 h after subcutaneous implantation of carrageenin-impregnated sponges. 3 Concentrations of the cyclo-oxygenase products prostaglandin E2 (PGE2), 6-oxo-PGF1α and thromboxane B2 (TXB2) in inflammatory exudates and serum (obtained from blood clotted at 37° C) were measured by specific radioimmunoassays. 4 TXB2 concentrations in exudates increased to about 100 ng ml−1 at 8 h but decreased to less than 20 ng ml−1 after 24 h. PGE2 concentrations increased from 4–12 h and remained between 80 and 120 ng ml−1 from 12–24 h. 6-oxo-PGF1α had the same time course as that of PGE2 but concentrations were approximately one third of PGE2 values. 5 TXB2 concentrations in serum from thrombocytopaenic rats were less than 5% of control values. Thrombocytopaenia did not affect TXB2, PGE2 or 6-oxo-PGF1α concentrations or total leukocyte numbers in inflammatory exudates. 6 Methotrexate-induced neutropaenia did not affect serum TXB2 concentrations but cyclo-oxygenase products (including TXB2) in 6 h inflammatory exudates were reduced by 60–95%. 7 Colchicine (1.0 mg kg−1 s.c.) prevented leukocyte accumulation in sponge exudates and this was accompanied by a reduction in TXB2, PGE2 and 6-oxo-PGF1α concentrations at 6 h. 8 These results indicate that platelets are the source of TXB2 in clotting blood but do not contribute to cyclo-oxygenase activity in experimental inflammation. The results also suggest that migrating leukocytes are the major source of thromboxane and to a lesser degree prostaglandins in acute 6 h inflammatory exudates.