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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-49463

Richter, V; Savery, M D; Gassmann, M; Baum, O; Damiano, E; Pries, A R (2011). Excessive erythrocytosis compromises the blood-endothelium interface in erythropoietin-overexpressing mice. Journal of Physiology, 589(21):5181-5192.

Accepted Version


Elevated systemic hematocrit (Hct) increases cardiovascular risk, such as stroke and myocardial infarction. One possible pathophysiological mechanism could be a disturbance of the blood - endothelium interface. It has been shown that blood interacts with the endothelial surface via a gel-like layer ('glycocalyx', or 'endothelial surface layer - ESL') that modulates various biological processes, including inflammation, permeability, and atherosclerosis. However, consequences of an elevated Hct on the functional properties of this interface are incompletely understood. In a transgenic mouse (tg6) model exhibiting systemic Hct levels of about 0.85 the glycocalyx/ESL was nearly abolished. The corresponding increase in vessel diameter had only minor effects on peripheral flow resistance. This suggests that the pathological effects of elevated Hct may relate stronger to the biological corollaries of a reduced ESL thickness and alterations of the blood-endothelium interface, than to an increased flow resistance.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Integrative Human Physiology
05 Vetsuisse Faculty > Institute of Veterinary Physiology
DDC:570 Life sciences; biology
610 Medicine & health
Deposited On:14 Sep 2011 06:46
Last Modified:27 Nov 2013 16:30
Additional Information:The definitive version is available at www.blackwell-synergy.com’ and www.jphysiol.org.
Publisher DOI:10.1113/jphysiol.2011.209262
PubMed ID:21859826
Citations:Web of Science®. Times Cited: 4
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Scopus®. Citation Count: 4

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