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Am J Physiol Heart Circ Physiol 276: H107-H114, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 1, H107-H114, January 1999

Influence of arteriovenular pairing on PAF-induced capillary filtration

Norman R. Harris, Georgia A. Morgan First, and Robert D. Specian

Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport, Louisiana 71130

The purpose of this study was to determine the basic mechanism by which leukocyte-endothelial cell adhesion mediates platelet-activating factor (PAF)-induced increases in capillary fluid filtration rate. A modified Landis technique was used to observe fluid filtration from capillaries in the rat mesentery. Hypothetical mechanisms of increased filtration that were tested included 1) a direct action of leukocytes on endothelial cells during transit through the capillaries; 2) an upstream propagated response (via gap junction communication by adjacent endothelial cells) originating at sites of venular leukocyte adhesion; and 3) venule-to-arteriole communication, where mediators produced at the site of venular leukocyte adhesion reach a nearby paired arteriole that delivers the mediators to branching capillaries. Evidence was obtained in opposition to the first two hypotheses. However, in support 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-arteriole communication might modify capillary filtration rate during acute inflammation.

microvascular permeability; adhesion molecule expression; endothelial barrier dysfunction; leukocyte-endothelial cell adhesion; acute inflammation; platelet-activating factor


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