Skip to main content
Fig. 5 | Critical Care

Fig. 5

From: Regulation of blood flow and volume exchange across the microcirculation

Fig. 5

The endothelial surface layer model. Left hand panel: An intact endothelial surface layer, consisting of the endothelial glycocalyx and attached plasma protein molecules, oncotically (thick black arrow) limits hydrostatically driven (thick white arrow) fluid movement across the vascular wall within the microvascular high-pressure segments, which, in addition to narrow interendothelial clefts with high resistance to water flow, allows for hardly any egress of colloidal particles and only very low net rates of fluid extravasation (thin black arrow; Πt and Πc are in equal ranges, but irrelevant because Πe (high) and Πg (low) count). Right hand panel: At the venular aspect, relatively free and easy exchange of colloidal particles is allowed in both directions across the vascular wall (black arrows). This is feasible, because the interstitial space of most organs and tissues is now known to possess oncotic and hydrostatic pressures close to those existing in the end- and post-capillary vessel segments (Πv – Πt is small, but Pv – Pt is also small). There is no need for largescale reabsorption, as suggested by Ernest Starling (according to Jacob et al. [41] and Becker et al. [28]). EC endothelial cell, ESL endothelial surface layer, IS interstitial space, Πc, e, g, t, and v oncotic pressure in capillary plasma, ESL, below the ESL, in the tissue, and venular space, respectively, Pc, t, and v hydrostatic pressure in the capillary, tissue, and venule, respectively

Back to article page