The adhesion molecule P-selectin and cardiovascular disease - cardiac surgical implications
Liverpool Heart And Chest Hospital, Liverpool, England, United KingdomEuropean Heart Journal (Impact Factor: 15.2). 07/2004; 25(11):993. DOI: 10.1016/j.ehj.2004.01.023
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ABSTRACT: Soluble adhesion molecules are considered to be markers of inflammation, endothelial activation, or damage. This study was designed to assess whether adhesion molecules are specifically altered in patients undergoing cardiac surgical procedures. Three groups of 20 patients each were prospectively studied: patients undergoing elective coronary artery bypass grafting; patients scheduled for a Whipple pancreatoduodenectomy; and patients undergoing elective pneumonectomy for lung cancer. Plasma levels of soluble adhesion molecules (endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and granule membrane protein 140) were measured from arterial blood samples after induction of anesthesia (baseline), at the end of the operation, 2 hours and 5 hours after operation, and on the morning of the first postoperative day. Duration of operation was longest in the group having a Whipple operation (289 +/- 50 minutes) and did not differ between the other two groups. Plasma levels of all measured adhesion molecules at baseline were within normal ranges. After cardiopulmonary bypass, levels of adhesion molecules were significantly increased in the cardiac surgical patients (soluble endothelial leukocyte adhesion molecule-1, from 38 +/- 11 ng/mL at baseline to 68 +/- 12 ng/mL; soluble intercellular adhesion molecule-1, from 241 +/- 50 ng/mL to 498 +/- 78 ng/mL; and granule membrane protein 140, from 69 +/- 12 ng/mL to 150 +/- 25 ng/mL). On the morning of the first postoperative day, all levels had returned to baseline except that of soluble vascular cell adhesion molecule-1, which was still elevated (p < 0.05). In both the other groups, concentrations of adhesion molecules remained almost unchanged. Cardiac operation was associated with increased plasma levels of soluble adhesion molecules, a finding indicating endothelial activation or dysfunction. In contrast, in patients undergoing complex, long-lasting abdominal or lung operations, soluble adhesion molecules remained unchanged. Activation of proinflammatory cascades, ischemia/reperfusion phenomenon, and microcirculatory dysfunction appear to be the most likely reasons for this difference between groups. Whether modulation of adhesion molecules may influence organ function after cardiopulmonary bypass remains to be elucidated in further studies.The Annals of Thoracic Surgery 03/1998; 65(3):608-14. DOI:10.1016/S0003-4975(97)01306-4 · 3.85 Impact Factor
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ABSTRACT: 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. 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. 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. 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.The Annals of Thoracic Surgery 09/2003; 76(2):453-8; discussion 458. DOI:10.1016/S0003-4975(03)00433-8 · 3.85 Impact Factor
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