The purpose of this study was to determine the basic mechanism by which leu
kocyte-endothelial cell adhesion mediates platelet-activating factor (PAF)-
induced increases in capillary fluid filtration rate. A modified Landis tec
hnique was used to observe fluid filtration from capillaries in the rat mes
entery. Hypothetical mechanisms of increased filtration that were tested in
cluded I) a direct action of leukocytes on endothelial cells during transit
through the capillaries; 2) an upstream propagated response (via gap junct
ion communication by adjacent endothelial cells) originating at sites of ve
nular leukocyte adhesion; and 3) venule-to-arteriole communication, where m
ediators produced at the site of venular leukocyte adhesion reach a nearby
paired arteriole that delivers the mediators to branching capillaries. Evid
ence was obtained in opposition to the first two hypotheses. However, in su
pport of the third hypothesis, a significant correlation was found between
the extent of arteriolar pairing to venules and the PAF-induced increase in
capillary fluid filtration rate. These findings suggest that venule-to-art
eriole communication might modify capillary filtration rate during acute in
flammation.