Bulat Marin, Klarica Marijan
Croat Med J. 2014 Aug 28;55(4):291-8.
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.
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.
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.
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.
毛细血管和组织间隙中的流体静压与胶体渗透压之间的关系用于解释液体透过微血管壁的滤过和重吸收。这些压力被纳入毛细血管的斯塔林胶体渗透压假说中，然而，当毛细血管流体静压较高（直立位时足部）和较低（肺部）时，或者当实验和某些临床状态（如遗传性低白蛋白血症）中血浆胶体渗透压显著降低时，该假说无法解释液体稳态。
为了解释液体稳态，我们提出了毛细血管的渗透反压假说，该假说认为：1）在动脉毛细血管中液体透过微血管壁滤过过程中，血浆溶质被筛分（保留），从而产生血浆渗透反压；2）这种渗透反压沿毛细血管长度升高，当它达到毛细血管流体静压时，水的滤过停止；3）在流体静压较低的静脉毛细血管和毛细血管后微静脉中，渗透反压有助于从组织间隙重吸收水分，这导致渗透反压消散。根据修正的范特霍夫方程，渗透反压的产生取决于血浆溶质浓度及其与水相比在微血管壁上的受限通过（反射系数）。
血浆氯化钠占血浆渗透压的83%，且在脑和外周连续毛细血管壁上的通过受限，因此钠和氯是产生渗透反压的最重要溶质。我们的计算表明，在不同的水滤过率下，氯化钠的渗透反压起到负反馈控制作用：较高的流体静压和水滤过率会产生较高的渗透反压，该反压对抗滤过并导致较高的水重吸收率。此外，我们的分析表明，动脉毛细血管中的液体体积变化与组织间隙液中的变化成比例地大100倍。
渗透反压假说解释了在高、平均和低毛细血管流体静压下的液体稳态。血浆蛋白和无机电解质分别对血浆渗透压贡献0.4%和94%，因此血浆蛋白的渗透压（胶体渗透压）较低，尽管它们在微血管壁上的通过受限程度较高，但与电解质相比，它们对渗透反压的形成贡献很小。然而，血浆蛋白的缺乏或浓度极低会增加微血管壁对水和溶质的通透性，损害渗透反压的形成，导致组织间隙水肿的发生。
