Plasma from patients undergoing coronary artery bypass graft surgery does not activate endothelial cells under shear stress in vitro.

Abstract

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.