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Journal of Thoracic and Cardiovascular Surgery
Article
License: Elsevier Non-Commercial
Data sources: UnpayWall
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Journal of Thoracic and Cardiovascular Surgery
Article . 2006
License: Elsevier Non-Commercial
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Journal of Thoracic and Cardiovascular Surgery
Article . 2006 . Peer-reviewed
License: Elsevier Non-Commercial
Data sources: Crossref
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Circulating endothelial cells demonstrate an attenuation of endothelial damage by minimizing the extracorporeal circulation

Authors: Skrabal, Christian A.; Choi, Yeong H.; Kaminski, Alexander; Steiner, Michael; Kundt, Guenther; Steinhoff, Gustav; Liebold, Andreas;

Circulating endothelial cells demonstrate an attenuation of endothelial damage by minimizing the extracorporeal circulation

Abstract

Detachment of endothelial cells may represent serious injury of the endothelium after cardiopulmonary bypass. We investigated whether the extent of endothelial injury is related to the type of cardiopulmonary bypass system used (conventional or minimized) and determined circulating endothelial cells as well as von Willebrand factor and soluble thrombomodulin.Twenty patients scheduled for elective coronary bypass grafting were randomly assigned to either the minimal extracorporeal circulation system or the standard cardiopulmonary bypass. Ten healthy volunteers served as controls. Circulating endothelial cells per milliliter of full blood were perioperatively determined by immunomagnetic cell separation technique. Endothelial plasma markers were measured by enzyme-linked immunosorbent assay.Preoperative circulating endothelial cell numbers did not differ between the experimental groups, but were significantly higher than in the healthy controls (18.6 +/- 5.6 vs 7.2 +/- 3.8, P < .001). At 6 hours, circulating endothelial cell numbers increased significantly compared with baseline in both experimental groups and peaked at 12 hours after cardiopulmonary bypass initiation, each time with significantly lower values in the minimal extracorporeal circulation group (6 hours: 44.0 +/- 9.9 vs 29.6 +/- 9.8, P = .007; 12 hours: 48.1 +/- 6.8 vs 31.8 +/- 7.1, P < .001). Likewise, von Willebrand factor and soluble thrombomodulin postoperatively increased in both groups with a tendency toward lower levels in the minimal extracorporeal circulation group. Although circulating endothelial cells gradually declined, continually with lower numbers in the minimal extracorporeal circulation group, the endothelial plasma markers remained elevated during observation time.Circulating endothelial cells represent a novel marker of the intrinsic endothelial damage caused by cardiopulmonary bypass. Its analysis facilitates the evaluation of cardiopulmonary bypass modifications as the minimal extracorporeal circulation system could be proven to be less injurious to endothelium and myocardium.

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Keywords

Pulmonary and Respiratory Medicine, Male, Cardiopulmonary Bypass, Thrombomodulin, Endothelial Cells, Cell Count, Pilot Projects, Cell Separation, Middle Aged, Cardiovascular Diseases, von Willebrand Factor, Humans, Surgery, Female, Endothelium, Vascular, Prospective Studies, Cardiology and Cardiovascular Medicine, Biomarkers, Aged

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
29
Average
Top 10%
Top 10%
hybrid