Capillary filtration and absorption are influenced by various factors. Arteriolar vasoconstriction can reduce capillary hydrostatic pressure (Pc) and promote absorption transiently. However, prolonged vasoconstriction leads to increased interstitial hydrostatic pressure (Pi) and diminished absorption. In some vascular beds, like the renal glomerulus, filtration occurs along the entire length of the capillary due to high hydrostatic pressure. In other beds, such as the intestinal mucosa, the balance of hydrostatic and oncotic forces favors absorption along the capillary.

Under normal conditions, the steady-state balance between precapillary resistance, interstitial fluid pressure, and plasma oncotic pressure ensures balanced filtration and absorption across the capillary wall. However, changes in precapillary resistance affect fluid movement. Vasoconstriction reduces net filtration, while vasodilation increases it.

In the lungs, capillary hydrostatic pressure is relatively low (around 8mmHg). With a plasma oncotic pressure of 25mmHg and interstitial fluid pressure of approximately 15mmHg, a slight net absorption occurs (fluid leaves the interstitial space). Despite net absorption, pulmonary lymph is formed due to osmotically withdrawn fluid from the capillaries. Pathological conditions, like left ventricular failure or mitral valve stenosis, can cause pulmonary capillary hydrostatic pressure to exceed plasma oncotic pressure, resulting in pulmonary edema and impaired gas exchange.

The rate of fluid movement across the capillary membrane (Qf) depends on the algebraic sum of hydrostatic and osmotic forces (ΔP), as well as the capillary wall area available for filtration (Am), the distance across the wall (Δx), the filtrate viscosity (η), and the filtration constant of the membrane (k). This can be expressed using Poiseuille's law for flow through tubes.

The capillary filtration coefficient (kt) represents the rate of filtration per unit weight of tissue. It incorporates the constant factors of capillary wall thickness and filtrate viscosity. Physiological conditions like arteriolar dilation or capillary distention, as well as adverse conditions like hypoxia, hypercapnia, or reduced pH, do not alter the filtration coefficient or capillary permeability. However, in cases of capillary injury, such as toxin exposure or severe burns, increased capillary permeability results in the leakage of fluid and protein into the interstitial space. This is reflected by an increase in the filtration coefficient.
Fig. 17.28 ). However, in well-perfused capillaries, arteriolar vasoconstriction can reduce Pc in such a way that absorption at the arteriolar end can occur transiently. With continued vasoconstriction, absorption diminishes with time because Pi increases. In some vascular beds (e.g., the renal glomerulus), hydrostatic pressure in the capillary is high enough to cause filtration along the entire length of the capillary. In other vascular beds (e.g., the intestinal mucosa), the hydrostatic and oncotic forces are such that absorption occurs along the whole capillary.
In the steady-state Pa, Pv, postcapillary resistance, hydrostatic and oncotic pressure of interstitial fluid, and oncotic pressure of plasma are relatively constant. Hence, in the normal state, filtration and absorption across the capillary wall are well balanced. However, a change in precapillary resistance influences fluid movement across the capillary wall. Vasoconstriction reduces net filtration, and vasodilation increases filtration.
Inthelungs,meancapillaryhydrostaticpressureisonlyapproximately8mmHg(see ).Becauseplasmaoncoticpressureis25mmHgandpressureoftheinterstitialfluidinthelungsisapproximately15mmHg,thenetforceslightlyfavorsnetabsorption(i.e.,fluidleavestheinterstitialspace).Despitenetabsorption,pulmonarylymphisformed.Thislymphconsistsoffluidthatisosmoticallywithdrawnfromthecapillariesbythesmallamountofplasmaproteinthatescapesthroughthecapillaryendothelium.Inpathologicalconditions,suchasleftventricularfailureormitralvalvestenosis,pulmonarycapillaryhydrostaticpressuremayexceedplasmaoncoticpressure.Whenthisoccurs,itmaycausepulmonaryedema,aconditioninwhichexcessivefluidaccumulatesinthepulmonaryinterstitium.Thisfluidaccumulationseriouslyinterfereswithgasexchangeinthelungs.
Capillary Filtration Coefficient. The rate of fluid movement (Qf) across the capillary membrane depends not only on the algebraic sum of the hydrostatic and osmotic forces across the endothelium (ΔP) but also on the area (Am) of the capillary wall available for filtration, the distance (Δx) across the capillary wall, the viscosity (η) of the filtrate, and the filtration constant (k) of the membrane. These factors may be expressed as follows:
Equation 17.21
This expression, which describes the flow of fluid through the membrane pores, is essentially Poiseuille’s law for flow through tubes.
Because the thickness of the capillary wall and the viscosity of the filtrate are relatively constant, they can be included in the filtration constant k. If the area of the capillary membrane is not known, the rate of filtration can be expressed per unit weight of tissue. Hence, the equation can be simplified as
Equation 17.22 where kt is the capillary filtration coefficient for a given tissue and the units for Qf are milliliters per minute per 100 g of tissue.
In any given tissue, the filtration coefficient per unit area of capillary surface, and hence capillary permeability, is not changed by various physiological conditions, such as arteriolar dilation and capillary distention, or by such adverse conditions as hypoxia, hypercapnia, or reduced pH. When capillaries are injured (as by toxins or severe burns), significant amounts of fluid and protein leak out of the capillaries into the interstitial space. This increase in capillary permeability is reflected by an increase in the filtration coefficient.