Capillary filtration during acute inflammation: role of adherent neutrophils.

Fluid filtration rate with respect to surface area (Jv/S) was measured in capillaries of rat mesentery by a micro-occlusion technique. Superfusion of the mesentery with 100 nM platelet-activating factor (PAF) caused a fivefold increase in Jv/S (control, mean +/- SE = 0.016 +/- 0.002 micron/s, n = 44 rats; PAF, 0.078 +/- 0.010, n = 10), whereas 20 nM leukotriene B4 (LTB4) had no effect (0.010 +/- 0.003, n = 8). These doses of PAF and LTB4 induced a similar level of leukocyte adherence to venular endothelium. Neutrophils play a role in PAF-mediated increases in Jv/S, since a significantly lower Jv/S was elicited by PAF superfusion in neutropenic rats (0.024 +/- 0.006, n = 7). Monoclonal antibodies (MAb) directed against either the leukocyte adhesion glycoprotein CD11/CD18 (0.037 +/- 0.006, n = 8) or the endothelial cell adhesion molecule P-selectin (0.025 +/- 0.004, n = 8) also attenuated PAF-induced capillary filtration, whereas a nonbinding form of the P-selection MAb had no inhibitory effect (0.066 +/- 0.024, n = 3). These results indicate that PAF, but not LTB4, enhances capillary fluid filtration rate. While neutrophils do not adhere to endothelium in capillaries exposed to PAF, they do appear to contribute significantly to the PAF-induced capillary fluid filtration.