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Updated: Oct 13, 2025
Human Saphenous Vein Endothelial Cell Isolation and Exposure to Controlled Levels of Shear Stress and Stretch
Published on: April 21, 2023
Plasma from patients undergoing coronary artery bypass graft surgery does not activate endothelial cells under shear
Sophie F Ellermann1,2,3,4, Thomas W L Scheeren3, Rianne M Jongman1,3
1Department of Pathology and Medical Biology, Oldenburg, Germany.
Insights
Coronary artery bypass graft surgery with cardiopulmonary bypass can cause kidney injury. Postoperative plasma did not increase endothelial inflammation markers in vitro, despite mild systemic inflammation observed in patients.
Area of Science:
- Cardiovascular Surgery
- Nephrology
- Immunology
Background:
- Coronary artery bypass graft surgery using cardiopulmonary bypass is linked to acute kidney injury.
- Microvascular endothelial inflammation is a potential mechanism contributing to kidney injury post-cardiac surgery.
Purpose of the Study:
- To investigate if plasma from patients undergoing coronary artery bypass graft surgery with cardiopulmonary bypass induces endothelial adhesion molecule expression.
- To assess the role of altered shear stress in this process using an in vitro model.
Main Methods:
- Analyzed clinical characteristics and markers of systemic inflammation and kidney injury in 29 patients pre and post-coronary artery bypass grafting with cardiopulmonary bypass.
- Investigated the effects of tumor necrosis factor-alpha and patient plasma on endothelial inflammation and adhesion markers in vitro.
Main Results:
- Plasma tumor necrosis factor-alpha levels increased post-surgery. Biomarkers for kidney injury, neutrophil gelatinase-associated lipocalin and kidney injury molecule-1, peaked at 6 and 24 hours post-operation, respectively.
- In vitro, tumor necrosis factor-alpha induced E-selectin, interleukin-8, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 expression.
- Postoperative plasma did not enhance endothelial inflammation or adhesion molecule expression under shear stress compared to control plasma.
Conclusions:
- Patients undergoing cardiopulmonary bypass surgery exhibit mild systemic inflammation and kidney injury.
- Despite observed inflammation, plasma components from these patients did not stimulate endothelial inflammation and adhesion molecule expression in vitro.
Background:
Cardiac surgery with cardiopulmonary bypass (CPB) is commonly associated with acute kidney injury, and microvascular endothelial inflammation is a potential underlying mechanism. We hypothesized that pro-inflammatory components of plasma from patients who underwent coronary artery bypass graft surgery with CPB induce endothelial adhesion molecule expression when incorporating altered shear stress in the in vitro model.
Methods:
The clinical characteristics and markers of systemic inflammation and kidney injury were analyzed pre and postoperatively in 29 patients undergoing coronary artery bypass grafting with CPB. The effects of tumor necrosis factor (TNF)-α and patient plasma on the expression of endothelial inflammation and adhesion markers were analyzed in vitro.
Results:
Plasma TNF-α was elevated 6 h postoperation (median: 7.3 pg/ml (range: 2.5-94.8 pg/ml)). Neutrophil gelatinase-associated lipocalin in plasma peaked 6 h (99.8 ng/ml (52.6-359.1 ng/ml)) and in urine 24 h postoperation (1.6 ng/mg (0.2-6.4 ng/mg)). Urinary kidney injury molecule-1 concentration peaked 24 h postoperation (0.5 ng/mg (0.2-1.2 ng/mg). In vitro, the expression of E-selectin was induced by 20 pg/ml TNF-α. In addition, the expression of interleukin-8, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 was induced by 100 pg/ml TNF-α. Compared to healthy control plasma exposure, postoperative plasma did not increase the expression of markers of endothelial inflammation and adhesion under shear stress in vitro.
Conclusion:
Patients undergoing CPB surgery showed mild systemic inflammation and kidney injury. However, the plasma components did not stimulate endothelial inflammation and adhesion molecule expression in vitro.
