In microvessels with continuous endothelium, the majority of transvascular Jv is presumed to occur via the inter-endothelial cell junctions. Numerous mathematical models have been proposed to describe the geometry of these pathways, including cylindrical pores, rectangular slits, and a fiber matrix model . Each of these models alone is unable to fully account for in vivo measures of volume and hydrophilic solute flux across microvessels. Of these models, the fiber matrix model appears to describe many of the transport coefficients measurable in vivo. The fiber matrix model is consistent with experiments involving disruption of the endothelial surface layer (glycocalyx). For example, perfusion of microvessels with cationized ferritin demonstrates a layer up to 100 nm thick on the endothelial cell surface. Exposure of microvessels to an enzyme, pronase, results in reduction of the thickness of this surface layer and a significant increase in microvessel L Similarly,
Jv: volume flux
Lp: hydraulic conductivity
S: surface area
Pc: capillary hydrostatic pressure Pi: interstitial hydrostatic pressure pc: capillary oncotic pressure ni: interstitial oncotic pressure s: reflection coefficient
Figure 1 Pressures responsible for fluid movement across a capillary, and modern form of the Starling equation for fluid filtration. See text for details.
Pressure (cm H2O)
Pressure (cm H2O)
Figure 2 Landis-Michel technique for measurement of hydraulic conductivity (Lp) in individually perfused microvessels. (A) Relative placement of microinstruments and calculation of fluid filtration rate per unit surface area (JJS) based on vessel radius and erythrocyte location and velocity. (B) Calculation of Lp based on measures of JJS at different hydrostatic pressures.
p microvessel perfusion with a solution devoid of proteins reduces the thickness of the surface layer and induces a significant increase in Lp (known as the "protein effect"). These studies support the notion that the glycocalyx (which may be modeled as a fiber matrix) contributes significantly to the microvascular barrier to volume flux. Based on recent electron microscopic observations suggesting the presence of a thick endothelial surface layer (200 to 500 nm), elaborate models of a fiber matrix overlying interendothelial cell clefts with junctional strand gaps have been proposed . Although these models describe many in vivo measures of transvascular volume and solute flux, their validity remains to be confirmed.
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