Fluid filtration and reabsorption across microvascular walls: control by oncotic or osmotic pressure? (secondary publication).

Aim: Relationships between hydrostatic and oncotic (colloid osmotic) pressures in both capillaries and interstitium are used to explain fluid filtration and reabsorption across microvascular walls. These pressures are incorporated in the Starling oncotic hypothesis of capillaries which fails, however, to explain fluid homeostasis when hydrostatic capillary pressure is high (in feet during orthostasis) and low (in lungs), or when oncotic plasma pressure is significantly decreased in experiments and some clinical states such as genetic analbuminaemia.

Methods: To explain fluid homeostasis we propose osmotic counterpressure hypothesis of capillaries which claims: 1) during water filtration across microvascular wall in arterial capillary, the plasma osmolytes are sieved (retained) so that plasma osmotic counterpressure is generated, 2) this osmotic counterpressure rises along the length of capillary and when it reaches capillary hydrostatic pressure the water filtration is halted, and 3) in venous capillaries and postcapillary venules where hydrostatic pressure is low, the osmotic counterpressure is instrumental in water reabsorption from interstitium what leads to dissipation of osmotic counterpressure. According to modified van’t Hoff’s equation the generation of osmotic counterpressure depends on plasma concentration of osmolytes and their restricted passage (reflection coefficient) across microvascular wall in comparison to water.

Results: Plasma NaCl makes 83% of plasma osmolarity and shows restricted passage across the walls of cerebral and peripheral continuous capillaries, so that Na and Cl are the most important osmolytes for generation of osmotic counterpressure. Our calculation indicates that at various rates of water filtration the osmotic counterpressure of NaCl acts as negative feedback control: higher hydrostatic pressure and water filtration rate create higher osmotic counterpressure which opposes filtration and leads to higher water reabsorption rate. Furthermore, our analysis indicates that fluid volume changes in arterial capillaries are proportionally 100 times larger than in interstial fluid.

Conclusion: The osmotic counterpressure hypothesis explains fluid homeostasis at high, mean and low capillary hydrostatic pressures. Plasma proteins and inorganic electrolytes contribute 0.4% and 94% to plasma osmolarity, respectively, so that plasma proteins have low osmotic (oncotic) pressure and despite high restriction of their passage across microvascular wall they contribute little to build up of osmotic counterpressure in comparison to electrolytes. However, absence or very low concentration of plasma proteins increases microvascular wall permeability to water and osmolytes compromising build up of osmotic counterpressure leading to development of interstial oedema.