ULTRASTRUCTURAL AND CYTOCHEMICAL EVALUATION OF SEPSIS-INDUCED CHANGESIN THE RAT PULMONARY INTRAVASCULAR MONONUCLEAR PHAGOCYTES

Sepsis stimulates an increase in the number and activity of mononuclea r phagocytes in systemic host-defence organs. The present study was co nducted to define the ultrastructural and cytochemical characteristics of the mononuclear phagocytes that sequester in the lung microvascula ture of septic rats, Fourteen rats were challenged with a single intra peritoneal injection of saline (0.5 ml/100 g), E. coli (2 x 10(7)/100 g) or glucan (4 mg/100 g), and euthanased 2, 4, or 7 d later. The lung s were inflation fixed and processed for transmission electron microsc opy. Cellular morphology was used to identify the intravascular mononu clear phagocytes and acid phosphatase (AcPase) expression was monitore d as an index of cellular differentiation and activation. Control rats contained a limited number of monocytes in the pulmonary vasculature. In contrast, large numbers of activated mononuclear phagocytes were s een in the microvasculature within 48 h of treatment with either micro bial product. The recruited pulmonary intravascular mononuclear phagoc ytes (PIMP) exhibited AcPase-reactive Golgi complexes, accumulation of secretory vesicles and other features of cell activation consistent w ith enhanced biosynthetic activity. Subsequent electron microscopy, co nducted 4 and 7 d posttreatment, suggested that a progressive decline in the number and activity of PIMPs then occurred. In order to quantif y the sepsis-induced accumulation of AcPase-positive PIMP, the experim ental challenges were repeated in 11 rats and, 48 h later, tissue samp les were evaluated by light microscopy for tartrate-insensitive acid p hosphatase. Control rats exhibited 0.148 +/- 0.107 AcPase-positive PIM P/alveoli. E. coil and glucan challenged animals exhibited significant (P < 0.01) increases in AcPase-positive mononuclear phagocytes, with 0.782+/-0.073 and 0.636+/-0.170 PIMP/alveoli respectively, The results demonstrate that focal sepsis stimulates a significant, but transient , recruitment of activated mononuclear phagocytes into the rat pulmona ry microvasculature.