Levick JR, Michel CC, et al.
Cardiovascular research. Date of publication 2010 Jul 15;volume 87(2):198-210.
1. Cardiovasc Res. 2010 Jul 15;87(2):198-210. doi: 10.1093/cvr/cvq062. Epub 2010
Mar 3.
Microvascular fluid exchange and the revised Starling principle.
Levick JR(1), Michel CC.
Author information:
(1)Physiology, Basic Medical Sciences, St George's Hospital Medical School,
London, UK.
Microvascular fluid exchange (flow J(v)) underlies plasma/interstitial fluid
(ISF) balance and oedematous swelling. The traditional form of Starling's
principle has to be modified in light of insights into the role of ISF pressures
and the recognition of the glycocalyx as the semipermeable layer of endothelium.
Sum-of-forces evidence and direct observations show that microvascular
absorption is transient in most tissues; slight filtration prevails in the
steady state, even in venules. This is due in part to the inverse relation
between filtration rate and ISF plasma protein concentration; ISF colloid
osmotic pressure (COP) rises as J(v) falls. In some specialized regions (e.g.
kidney, intestinal mucosa), fluid absorption is sustained by local epithelial
secretions, which flush interstitial plasma proteins into the lymphatic system.
The low rate of filtration and lymph formation in most tissues can be explained
by standing plasma protein gradients within the intercellular cleft of
continuous capillaries (glycocalyx model) and around fenestrations. Narrow
breaks in the junctional strands of the cleft create high local outward fluid
velocities, which cause a disequilibrium between the subglycocalyx space COP and
ISF COP. Recent experiments confirm that the effect of ISF COP on J(v) is much
less than predicted by the conventional Starling principle, in agreement with
modern models. Using a two-pore system model, we also explore how relatively
small increases in large pore numbers dramatically increase J(v) during acute
inflammation.
DOI: 10.1093/cvr/cvq062
PMID: 20200043 [Indexed for MEDLINE]
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