Abstract

The effects of dexamethasone administration (5-9 mg/kg in 1-3 intraperitoneal injections) on the eosinophilic leukocyte population of various rat tissues (intestine, stomach, spleen, lung, bone marrow) have been studied by quantitative methods involving 1) direct cell counts in cell suspensions or tissue sections and 2) estimates of phospholipase B activity in tissue homogenates. The results confirm the technical premise that phospholipase B is a quantitative indicator of the eosinophilic leukocyte population of tissues and that the approach is applicable to experimental conditions of pronounced eosinopenia or eosinophilia. The action of the corticosteroid is seen to consist of an initial accumulation of eosinophils in the marrow (days 0-2) coinciding with a peripheral loss and probable destruction of these cells. An intermediate phase of rapid decline in marrow eosinophils, transient blood eosinophilia and the beginning of peripheral recovery ensues (days 2-4) and eventually progresses into a general pattern of recovery involving all eosinophil pools. In the stomach the recovery phase is characterized by a striking but brief phase of intense eosinophilia. Block of eosinophil release, peripheral loss and migration of cells from marrow to other tissues appear to be the major factors governing the response to corticoid administration.