The endothelial glycocalyx has been identified as a barrier to transvascular exchange of fluid, macromolecules, and leukocyte-endothelium (EC) adhesion during the inflammatory process. Shedding of glycans and structural changes of the glycocalyx have been shown to occur in response to several agonists. To elucidate the effects of glycan shedding on microvascular hemodynamics and capillary resistance to flow, glycan shedding in microvessels in mesentery (rat) was induced by superfusion with 10-7 M fMLP. Shedding was quantified by reductions of fluorescently labeled lectin (BS-1) bound to the EC and reductions in thickness of the barrier to infiltration of 70 kDa dextran (Dx70) on the EC surface. Red cell velocities (two-slit technique), pressure drops (dual servo-null method), and capillary hematocrit (direct cell counting) were measured in parallel experiments. The results indicate that fMLP caused shedding of glycans in all microvessels with reductions in thickness of the barrier to Dx70 of 110, 80 and 123 nm, in arterioles, capillaries and venules, respectively. Intravascular volumetric flows fell proportionately in all three divisions in response to rapid obstruction of venules by WBC-EC adhesion, and capillary resistance to flow rose 18% due to diminished deformability of activated WBCs. Capillary resistance fell significantly 26% over a 30 min period, as glycans were shed from the EC surface to increase effective capillary diameter while capillary hematocrit and anatomical diameter remained invariant. This decrease in capillary resistance mitigates the increase in resistance due to diminished WBC deformability and hence these concurrent rheological events may be of equal importance in affecting capillary flow during the inflammatory process.
- Glycocalyx thickness
- Copyright © 2011, American Journal of Physiology - Heart and Circulatory Physiology