Carrageenan-induced acute aseptic peritonitis was used as a model of inflammation. In rats with irradiation-induced leukopenia, the immediate and delayed phases of increased vascular permeability in the inflammatory focus were mediated by leukocytes. In the immediate phase, lysosomal enzymes, reactive oxygen species, and cyclooxygenase and lipoxygenase metabolites of arachidonic acid are involved in the regulation of vascular permeability, while in the delayed phase, lysosomal enzymes and lipoxygenase derivatives play the major role. Dexamethasone sharply inhibits vascular permeability in both phases.
Key Words: inflammation," vascular permeability; leukocytes; dexamethasoneOur previous experiments showed that irradiation-or vinblastine-induced leukopenia modulates vascular permeability (VP) in the inflammatory focus during the exudative phase by reducing the immediate phase (IP) and delayed phase (DP) of its increase. However, in the late exudative phase, VP was higher than during natural inflammation. These changes in VP correlated with leukocyte count in the inflammatory focus and peripheral blood [5,8].Here we studied the role of leukocytes in the regulation of VP during inflammation. VP in the inflammatory focus was determined in IP and DP of its increase during the recruitment of blood leukocytes in leukopenic animals and the use of lysosomal proteinase inhibitors, reactive oxygen species, cyclooxygenase, and lipoxygenase. The effects of dexamethasone on VP in the inflammatory focus were evaluated.
MATERIALS AND METHODSExperiments were performed on 72 male Wistar rats weighing 180-200 g. Acute aseptic peritonitis induced by intraperitoneal injection of 5 mg )~-carrageenan (Sigma) in 1 ml isotonic NaCI was used as a model of inflammation [6]. Four days before peritonitis,