Sodium arachidonate induced in vitro polymorphonuclear leukocyte aggregation.
Human polymorphonuclear leukocytes (PMNs) aggregated to sodium arachidonate (AA) in a dose dependent manner. Other agents such as epinephrine, or ADP were unable to initiate aggregation. The cells released lactate dehydrogenase (LDH) during aggregation, and electron microscopy demonstrated distinct morphologic changes in PMNs aggregated with AA. Indomethacin enhanced AA induced aggregation, whereas 1-methylimidazole inhibited aggregation and LDH release. Preincubation with cytochalasin B (CTB) did not enhance AA induced aggregation, nor did it reduce LDH release. Also, the effects of indomethacin or 1-methylimidazole on AA induced aggregation were unaltered by the presence of CTB. The results indicate that 1) LDH release occurs as a function of the aggregation process rather than a non-specific effect, 2) competition between cyclooxygenase and lipoxygenase occurs and 3) shifting this competition in favor of lipoxygenase enhances the PMN aggregation process.
D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology*; D002449:Cell Aggregation / Q000187:drug effects; D003571:Cytochalasin B / Q000494:pharmacology; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008854:Microscopy, Electron; D009504:Neutrophils / Q000187:drug effects* / Q000648:ultrastructure
D001095:Arachidonic Acids; D007093:Imidazoles; D016718:Arachidonic Acid; D003571:Cytochalasin B; D007770:L-Lactate Dehydrogenase; C018100:1-methylimidazole; D007213:Indomethacin