The endothelial glycocalyx affords compatibility of Starling's principle and high cardiac interstitial albumin levels.
OBJECTIVE
To test the role of an oncotic pressure gradient across the endothelial glycocalyx with respect to extravasation of fluid and colloids and development of tissue edema in a whole organ setting.


METHODS
We measured filtration in the intact coronary system of isolated guinea pig hearts, comparing colloid-free perfusion and perfusion with 1.67% albumin or 2% hydroxyethylstarch (oncotic pressures 5.30 vs. 11.10 mm Hg, respectively). Heparinase was used to alter the endothelial glycocalyx.


RESULTS
Extremely high net organ hydraulic conductivity was obtained with colloid-free perfusion (9.14 microl/min/g tissue). Supplementing perfusate with albumin caused a significant decrease, also vs. hydroxyethylstarch (1.04 vs. 2.67 microl/min/g, p < 0.05). Albumin also lowered edema formation vs. the other perfusion modes (p < 0.05). Stripping the glycocalyx of heparan sulfate reduced the effect of colloids, especially that of albumin. The steady-state concentrations of hydroxyethylstarch and albumin in the mixed interstitial fluid leaving the intact coronary bed averaged about 95% of the intravascular level. Electron and light microscopy indicated that colloid extravasated mainly in the venular sections.


CONCLUSIONS
We propose a low-filtration model for the coronary system with different barrier properties in arteriolar/capillary and venular sections. Arteriolar/capillary: very little fluid and colloid extravasation due to the endothelial surface layer formed by the glycocalyx and albumin plus the endothelial strand barrier; venular: little net extravsation of fluid and colloids despite large pores, because of low hydrostatic and oncotic pressure differences between intra- and extravascular spaces. The latter sites provide physiological access of large solutes (colloids) to the tissue.
Jacob
Matthias
M
Clinic of Anesthesiology, Ludwig-Maximilians University Munich, Nussbaumstr. 20, D-80336 Munich, Germany. matthias.jacob@med.uni-muenchen.de
Bruegger
Dirk
D
Rehm
Markus
M
Stoeckelhuber
Mechthild
M
Welsch
Ulrich
U
Conzen
Peter
P
Becker
Bernhard F
BF
D000418:Albumins / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport; D002199:Capillary Permeability; D003327:Coronary Disease / Q000378:metabolism* / Q000473:pathology; D003331:Coronary Vessels / Q000648:ultrastructure; D004487:Edema / Q000378:metabolism* / Q000473:pathology; D004573:Electrolytes / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000648:ultrastructure; D045604:Extracellular Fluid / Q000378:metabolism*; D005122:Exudates and Transudates / Q000378:metabolism; D019276:Glycocalyx / Q000378:metabolism* / Q000648:ultrastructure; D006168:Guinea Pigs; D019763:Heparin Lyase; D007150:Immunohistochemistry; D008854:Microscopy, Electron; D023421:Models, Animal; D010477:Perfusion; D011312:Pressure; D013213:Starch / Q000494:pharmacology; D014699:Venules
D000418:Albumins; D004573:Electrolytes; D013213:Starch; D019763:Heparin Lyase