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Am J Physiol Heart Circ Physiol (July 22, 2005). doi:10.1152/ajpheart.00297.2005
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Submitted on March 25, 2005
Accepted on July 18, 2005

Microvascular blood viscosity in vivo and the endothelial surface layer

Axel R Pries1* and Tim W Secomb2

1 Physiology, Charite, Berlin, Berlin, Germany; Anaesthesiology, Deutsches Herzzentrum Berlin, Berlin, Berlin, Germany
2 Physiology, University of Arizona, Tucson, Arizona, USA

* To whom correspondence should be addressed. E-mail: axel.pries{at}charite.de.

The apparent viscosity of blood in glass tubes declines with decreasing diameter (Fahraeus- Lindqvist effect) and exhibits a distinctive minimum between 6 and 7 µm. However, flow resistance in vivo in small vessels is substantially higher than predicted by in vitro viscosity data. The presence of a thick endothelial surface layer (ESL) has been proposed as the primary cause for this discrepancy. Here, a physical model is proposed for microvascular flow resistance as a function of vessel diameter and hematocrit in vivo, combining in vitro blood viscosity with effects of a diameter-dependent ESL. The model was developed based on observed flow distributions in three microvascular networks in the rat mesentery with 392, 546 and 383 vessel segments, for which vessel diameters, network architecture, flow velocity and hematocrit were determined by intravital microscopy. A previously described hemodynamic simulation was used to predict the distributions of flow and hematocrit from the assumed model for effective blood viscosity. The dependence of ESL thickness on vessel diameter was estimated by minimizing deviations of predicted values for velocities, flow directions and hematocrits from measured data. Optimal results were obtained with a layer thickness between about 0.8 and 1 µm for vessel diameters ranging from 10 to 40 µm, declining strongly for smaller diameters, with an additional hematocrit-dependent impact on flow resistance exhibiting a maximum for vessel diameters around 10 µm. These results show that flow resistance in vivo can be explained by in vitro blood viscosity and the presence of an ESL, and indicate the rheologically effective thickness of the ESL in microvessels.




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