readily permeable to ions, the ions have no
significant effect on osmotic pressure within
the capillary. Instead, the osmotic pressure is
principally determined by plasma proteins that
are relatively impermeable. Rather than being
this pressure is
referred to as the “oncotic” pressure or “colloid
osmotic” pressure because it is generated by
macromolecular colloids. Albumin, the most
abundant plasma protein, generates about 70%
of the oncotic pressure; globulins and fibrino-
gen generate the remainder of the oncotic pres-
sure. The plasma oncotic pressure typically is
25 to 30 mm Hg. When capillaries are filtering
fluid, the oncotic pressure increases along the
length of the capillary, particularly in capillar-
ies having high filtration rates (e.g., renal glo-
merular capillaries). This occurs because the
filtered fluid leaves behind proteins, increasing
the plasma protein concentration.
When oncotic pressure is determined, it is
measured across a semipermeable membrane,
that is, a membrane that is permeable to fluid
and electrolytes but not permeable to large
protein molecules. In most capillaries, how-
ever, the endothelial barrier has a finite perme-
ability to proteins. The actual permeability to
proteins depends on the type of capillary and
on the nature of the proteins (size, shape, and
charge). Because of this finite permeability, the
effective oncotic pressure generated across the
capillary membrane is less than that calculated
from the protein concentration. The reflection
coefficient (o ) across a capillary wall repre-
sents the effective oncotic pressure divided
by the oncotic pressure measured with a true
semipermeable membrane. If the capillary is
impermeable to protein, o = 1. If the capillary is
freely permeable to protein, o = 0. Continuous
capillaries have a high o (>0.9), whereas dis-
continuous capillaries (e.g., liver and spleen),
which are very “leaky” to proteins, have a rela-
tively low o . In the latter case, plasma and tis-
sue oncotic pressures may have a negligible
influence on the NDE If the capillary endothe-
lium becomes damaged by physical injury or
inflammation, the reflection coefficient may
decrease significantly, which reduces the abil-
ity of plasma oncotic pressure to oppose filtra-
tion, thereby increasing net filtration.
The tissue (or interstitial) oncotic pressure
(n.), a force that promotes filtration, is deter-
mined by the interstitial protein concentration
and the reflection coefficient of the capillary
wall for those proteins. The protein concen-
tration is influenced, in part, by the amount
of fluid filtration into the interstitium. For
example, increased capillary filtration into the
interstitium decreases interstitial protein con-
centration and reduces the oncotic pressure.
This effect of filtration on protein concentra-
tion serves as a mechanism to limit excessive
capillary filtration.
The interstitial oncotic
pressure, which is typically about 5 mm Hg,
acts on the capillary fluid to enhance filtration
and oppose reabsorption; therefore, when the
interstitial proteins are diluted and this pres-
sure falls, filtration is reduced. The interstitial
protein concentration is also determined by
the capillary permeability to protein. If this is
increased, for example, by vascular damage or
inflammation, then more proteins will be fil-
tered with the fluid into the interstitium. An
increase in interstitial protein concentration
facilitates net filtration by reducing the net
force for reabsorption.
Together, the hydrostatic and oncotic forces are
related to the NDF as shown in Equation 8-4
and in Figure 8.7. The net hydrostatic pres-
is represented by (Pc - P.). The net oncotic
pressure, which promotes reabsorption, is
represented by (nc - tc.), multiplied by the
reflection coefficient (a ). This equation shows
that the NDF is increased by increases in Pc
and n. and decreased by increases in P. and n .
Eq. 8-4
NDF = (Pc - P )-a (n c-n,)
If the above expression for NDF is incorpo-
rated into Equation 8-2, the following equa-
tion is derived, which is sometimes referred to
as the Starling equation:
Eq. 8-5
J = Kf • A [(Pc - P,) - a ( ^ -n,)]
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