Premium
Excessive erythrocytosis compromises the blood–endothelium interface in erythropoietin‐overexpressing mice
Author(s) -
Richter Vincent,
Savery Michele D.,
Gassmann Max,
Baum Oliver,
Damiano Edward R.,
Pries Axel R.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.209262
Subject(s) - glycocalyx , endothelium , blood flow , vascular permeability , inflammation , medicine , pathophysiology , erythropoietin , immunology , endocrinology
Non‐Technical Summary Elevated systemic haematocrit (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 (the ‘glycocalyx’, or ‘endothelial surface layer’– ESL) that modulates various biological processes, including inflammation, permeability and atherosclerosis. However, the 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 more strongly to the biological corollaries of a reduced ESL thickness and alterations of the blood–endothelium interface than to an increased flow resistance.