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Ann Thorac Surg 2003;76:453-458
© 2003 The Society of Thoracic Surgeons

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Original article: cardiovascular

Pressure distension stimulates the expression of endothelial adhesion molecules in the human saphenous vein graft

^a Department of Cardiovascular Sciences, Interdisciplinary Center for Biomedical Research (CIR), University Campus BioMedico di Roma, Rome, Italy
^b Department of Clinical and Experimental Medicine, University of Catanzaro, Catanzaro, Italy

Accepted for publication February 21, 2003.

^* Address reprint requests to Dr Chello, Department of Cardiovascular Sciences, Unit of Cardiac Surgery, Università Campus BioMedico di Roma, Via E. Longoni 83, Rome 00155, Italy.
e-mail: m.chello{at}unicampus.it

BACKGROUND: Mechanical trauma occurring during saphenous vein graft harvesting plays a major role in graft failure after coronary bypass surgery. There is increasing evidence that neutrophil–endothelial interaction is involved in the pathogenesis of early graft occlusion. This study evaluates the effect of pressure distension on the expression of endothelial adhesion molecules in human saphenous vein.

METHODS: Segments of saphenous vein graft (SVG) were collected from 20 patients undergoing coronary bypass surgery. We evaluated the expression of intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1), and P-selectin on SVG endothelium under basal conditions and after pressure distension at 300 mm Hg. In the same experimental setting we also evaluated adhesion of both unstimulated and activated neutrophils to the endothelium of SVG.

RESULTS: Control endothelial cells exhibited only a weak staining for intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1), and P-selectin, whereas the levels of adhesion molecules increased significantly in the distended veins. Similarly, significantly greater adhesion of both unstimulated and activated neutrophils was observed in distended veins compared with control veins.

CONCLUSIONS: Pressure distension of SVG before coronary bypass surgery induces upregulation of endothelial adhesion molecules, with subsequent increase in neutrophil adhesion to the endothelium. Neutrophil adhesion to endothelial cells may contribute to early failure of SVG.

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