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 μl/min/g tissue). Supplementing perfusate with albumin caused a significant decrease, also vs. hydroxyethylstarch (1.04 vs. 2.67 μl/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. Conclusion: 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. © 2006 Elsevier B.V. All rights reserved.
Jacob, M., Bruegger, D., Rehm, M., Stoeckelhuber, M., Welsch, U., Conzen, P., & Becker, B. F. (2007). The endothelial glycocalyx affords compatibility of Starling’s principle and high cardiac interstitial albumin levels. Cardiovascular Research, 73(3), 575–586. https://doi.org/10.1016/j.cardiores.2006.11.021