Secretion of a hyperemia-inducing moiety by mitogen or glycogen stimulated mononuclear inflammatory cells of sheep and rabbit.

A nonlymphokine mediator of hyperemia has been shown to be secreted by both rabbit peritoneal exudate cells stimulated with 5% glycogen and by concanavalin A treated cells from afferent lymph of sheep. This mediator is not stored in an active form in cells, but is either activated or synthesized de novo in response to antigenic or mitogenic stimuli. Secretion of the mediator is inhibited by culturing cells in the presence of dexamethasone but not indomethacin. However, expression of the activity is inhibited by pretreatment of the assay animals with indomethacin, suggesting a two-step induction of hyperemia. A similar mediator was found to be secreted by sheep and rabbit alveolar lavage cells, and rat peritoneal exudate cells. The presence of this hyperemia-inducing activity from diverse species suggests a fundamental role in controlling blood flow. Alteration of blood flow may modulate delivery of blood-borne cells and factors to sites of chronic inflammation.