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Endothelial Exchange Processes  sults in only transient reabsorption. After several
                                       minutes it stops because the interstitial oncotic pres-
       Nutrients and waste products are exchanged  sure rises due to “self-regulation”. Thus, a major part
       across the walls of the capillaries and post-  of the 18 L/d expected to be reabsorbed from the ex-
       papillary venules (exchange vessels; ! p. 188).  change vessels (see above) might actually be reab-
                                       sorbed in the lymph nodes. Rhythmic contraction of
       Their endothelia contain small (ca. 2–5 nm) or  the arterioles (vasomotion) may also play a role by
       large (20–80 nm, especially in the kidneys and  decreasing P eff and thus by allowing intermittent
       liver) functional pores: permeable, intercellu-  capillary reabsorption.
       lar fissures or endothelial fenestrae, respec-  In parts of the body below the heart, the effects of
       tively. The degree of endothelial permeability  hydrostatic pressure from the blood column in-
       varies greatly from one organ to another. Vir-  crease the pressure in the capillary lumen (in the feet
       tually all endothelia allow water and inorganic  ! 90 mmHg). The filtration rate in these regions
                                       therefore rise, especially when standing still. This is
       ions to pass, but most are largely impermeable  counteracted by two “self-regulatory” mechanisms:
    Cardiovascular System  passage of certain larger molecules.  the capillaries (normally the case in glomerular capil-
       to blood cells and large protein molecules.
                                       (1) the outflow of water results in an increase in the
       Transcytosis and carriers (! p. 26f.) allow for
                                       luminal protein concentration (and thus ∆π) along
                                       laries, ! p. 152); (2) increased filtration results in an
         Filtration and reabsorption. About 20 L/day
                                       increase in P int and a consequent decrease in ∆P.
       of fluid is filtered (excluding the kidneys) into
                                        Edema. Fluid will accumulate in the interstitial
       the interstitium from the body’s exchange ves-
                                       space (extracellular edema), portal venous system
       sels. About 18 L/day of this fluid is thought to be
                                       edema) if the volume of filtered fluid is higher than
       The remaining 2 L/day or so make up the lymph
                                       the amount returned to the blood.
    8  reabsorbed by the venous limb of these vessels.  (ascites), and pulmonary interstice (pulmonary
       flow and thereby return to the bloodstream
       (! A). The filtration or reabsorption rate Q f is a  Causes of edema (! B):
                                       ! Increased capillary pressure (! B1) due to precapil-
       factor of the endothelial filtration coefficient K f  lary vasodilatation (P cap"), especially when the capil-
       (= water permeability k · exchange area A) and  lary permeability to proteins also increases (σ prot #
       the effective filtration pressure P eff (Q f = K f · P eff).  and ∆π #) due, for example, to infection or anaphy-
       P eff is calculated as the hydrostatic pressure  laxis (histamine etc.). Hypertension in the portal vein
       difference ∆P minus the oncotic pressure  leads to ascites.
       difference ∆π across the capillary wall (Star-  ! Increased venous pressure (P cap ", ! B2) due, for
       ling’s relationship; ! A), where ∆P = capillary  example, to venous thrombosis or cardiac insuffi-
                                       ciency (cardiac edema).
       pressure (P cap) minus interstitial pressure (P int,  ! Decreased concentration of plasma proteins, es-
       normally ! 0 mmHg). At the level of the heart,  pecially albumin, leading to a drop in ∆π (! B3 and
       ∆P at the arterial end of the systemic capillar-  p. 379 A) due, for example, to loss of proteins (pro-
       ies is about 30 mmHg and decreases to about  teinuria), decreased hepatic protein synthesis (e.g.,
       22 mmHg at the venous end. Since ∆π (ca.  in liver cirrhosis), or to increased breakdown of
       24 mmHg; ! A) counteracts ∆P, the initially  plasma proteins to meet energy requirements
       high filtration rate (P eff = + 6 mmHg) is thought  (hunger edema).
                                       ! Decreased lymph drainage due, e.g., to lymph tract
       to change into reabsorption whenever P eff be-  compression (tumors), severance (surgery), oblitera-
       comes negative. (Since ∆P is only 10 mmHg in  tion (radiation therapy) or obstruction (bilharziosis)
       the lungs, the pulmonary P eff is very low). ∆π  can lead to localized edema (! B4).
       occurs because the concentration of proteins  ! Increased hydrostatic pressure promotes edema
       (especially albumin) in the plasma is much  formation in lower regions of the body (e.g., in the
       higher than their interstitial concentration.  ankles; ! B).
       The closer the reflection coefficient of the  Diffusion. Although dissolved particles are
       plasma proteins (σ prot) to 1.0, the higher ∆π  dragged through capillary walls along with fil-
       and, consequently, the lower the permeability  tered and reabsorbed water (solvent drag;
       of the membrane to these proteins (! p. 377).  ! p. 24), diffusion plays a much greater role in
       According to Starling’s relationship, water reab-  the exchange of solutes. Net diffusion of a sub-
  208  sorption should occur as long as P eff is negative.  stance (e.g., O 2, CO 2) occurs if its plasma and in-
       However, recent data suggest that a negative P eff re-  terstitial conc. are different.
       Despopoulos, Color Atlas of Physiology © 2003 Thieme
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