Endothelial hyperpermeability after cardiac surgery with cardiopulmonary bypass as assessed using an in vitro bioassay for endothelial barrier function

The mechanisms causing increased endothelial permeability after cardiopulmonary bypass (CPB) have not been elucidated. Using a bioassay for endothelial barrier function, we investigated whether endothelial hyperpermeability is associated with alterations in plasma endothelial activation and adhesion...

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Published in:	British journal of anaesthesia : BJA Vol. 116; no. 2; pp. 223 - 232
Main Authors:	Koning, N.J., Overmars, M.A.H., van den Brom, C.E., van Bezu, J., Simon, L.E., Vonk, A.B.A., Girbes, A.R.J., van Nieuw Amerongen, G.P., Boer, C.
Format:	Journal Article
Language:	English
Published:	England Elsevier Ltd 01-02-2016 Oxford University Press
Subjects:	Aged Aged, 80 and over Biological Assay - methods capillary permeability Capillary Permeability - physiology Cardiac Surgical Procedures Cardiopulmonary Bypass Endothelial Cells - physiology endothelium, vascular Endothelium, Vascular - physiology Enzyme-Linked Immunosorbent Assay Female haemodilution Humans In Vitro Techniques Male Middle Aged pulsatile flow Pulsatile Flow - physiology Random Allocation cardiopulmonary bypass endothelium, vascular haemodilution pulsatile flow capillary permeability
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Summary:	The mechanisms causing increased endothelial permeability after cardiopulmonary bypass (CPB) have not been elucidated. Using a bioassay for endothelial barrier function, we investigated whether endothelial hyperpermeability is associated with alterations in plasma endothelial activation and adhesion markers and can be attenuated by the use of pulsatile flow during CPB. Patients undergoing cardiac surgery were randomized to non-pulsatile (n+20) or pulsatile flow CPB (n+20). Plasma samples were obtained before (pre-CPB) and after CPB (post-CPB), and upon intensive care unit (ICU) arrival. Changes in plasma endothelial activation and adhesion markers were determined by enzyme-linked immunosorbent assay. Using electric cell–substrate impedance sensing of human umbilical vein endothelial monolayers, the effects of plasma exposure on endothelial barrier function were assessed and expressed as resistance. Cardiopulmonary bypass was associated with increased P-selectin, vascular cell adhesion molecule-1, and von Willebrand factor plasma concentrations and an increase in the angiopoietin-2 to angiopoietin-1 ratio, irrespective of the flow profile. Plasma samples obtained after CPB induced loss of endothelial resistance of 21 and 23% in non-pulsatile and pulsatile flow groups, respectively. The negative effect on endothelial cell barrier function was still present with exposure to plasma obtained upon ICU admission. The reduction in endothelial resistance after exposure to post-CPB plasma could not be explained by CPB-induced haemodilution. The change in the plasma fingerprint during CPB is associated with impairment of in vitro endothelial barrier function, which occurs irrespective of the application of a protective pulsatile flow profile during CPB. NTR2940.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0007-0912 1471-6771
DOI:	10.1093/bja/aev411