Barry, M. C.,Wang, J. H.,Kelly, C. J.,Sheehan, S. J.,Redmond, H. P.,BouchierHayes, D. J.;

1997

European Journal Of Vascular And Endovascular Surgery

Plasma factors augment neutrophil and endothelial cell activation during aortic surgery

Validated

()

13

44

381

387381

Lung injury following reperfusion results from endothelial damage caused by release of cytotoxic products by activated neutrophils (PMN) in the pulmonary microvasculature. This process is facilitated by the release of pro-inflammatory cytokines and arachidonic metabolites following the onset of reperfusion. This study aimed to evaluate the effect of plasma obtained before and after revascularisation on neutrophil and endothelial cell activation. Plasma (IR plasma) was obtained from venous blood samples taken before and during aortic cross-clamping, and 5, 40 and 60 min following clamp removal in seven patients undergoing elective infrarenal aortic aneurysm resection. PMN from healthy volunteers (n=5) were incubated with these plasma samples or with fMLP (N-formylmethionyl-leucyl-phenylalanine) as positive control for 30 min and assessed flow-cytometrically for CD11b expression. Human endothelial cells (ECV-304) were incubated with IR plasma for 2, 4, and 6 h or with tumour necrosis factor (TNF) (20 ng/ml) as positive control and assessed for ICAM-1 expression. Incubation with IR plasma resulted in a significant increase for pre-clamp in PMN CD11b expression. A similar trend was seen in endothelial cell ICAM-1 expression following 2 h incubation. These results indicate that reperfusion-induced endothelial dysfunction may be mediated by plasma factors released upon revascularisation which facilitate neutrophil-endothelial interaction through up-regulation of adhesion receptor expression.Lung injury following reperfusion results from endothelial damage caused by release of cytotoxic products by activated neutrophils (PMN) in the pulmonary microvasculature. This process is facilitated by the release of pro-inflammatory cytokines and arachidonic metabolites following the onset of reperfusion. This study aimed to evaluate the effect of plasma obtained before and after revascularisation on neutrophil and endothelial cell activation. Plasma (IR plasma) was obtained from venous blood samples taken before and during aortic cross-clamping, and 5, 40 and 60 min following clamp removal in seven patients undergoing elective infrarenal aortic aneurysm resection. PMN from healthy volunteers (n=5) were incubated with these plasma samples or with fMLP (N-formylmethionyl-leucyl-phenylalanine) as positive control for 30 min and assessed flow-cytometrically for CD11b expression. Human endothelial cells (ECV-304) were incubated with IR plasma for 2, 4, and 6 h or with tumour necrosis factor (TNF) (20 ng/ml) as positive control and assessed for ICAM-1 expression. Incubation with IR plasma resulted in a significant increase for pre-clamp in PMN CD11b expression. A similar trend was seen in endothelial cell ICAM-1 expression following 2 h incubation. These results indicate that reperfusion-induced endothelial dysfunction may be mediated by plasma factors released upon revascularisation which facilitate neutrophil-endothelial interaction through up-regulation of adhesion receptor expression.

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