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J Thorac Cardiovasc Surg 2002;124:758-767
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Endothelial expression of intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 is suppressed by postbypass plasma containing increased soluble intercellular adhesion molecule 1 and vascular cell adhesion molecule 1

Michael P. Vallely, MBBSa,b,c, Paul G. Bannon, FRACS, PhDb,c, Clifford F. Hughes, AO, FRACSb,c, Leonard Kritharides, FRACP, PhDa,d

From the Clinical Research Group, The Heart Research Institute,a the Cardiothoracic Surgical Unit Royal Prince Alfred Hospital,b The Baird Institute for Heart and Lung Research,c and the Department of Cardiology,d Concord Hospital, Sydney, Australia.

Supported by The Royal Australasian College of Surgeons' Foundation and Strathfield Private Hospital.

Received for publication Aug 20, 2001. Revisions requested Oct 26, 2001; revisions received Nov 9, 2001. Accepted for publication Jan 8, 2002. Address for reprints: Michael Vallely, MBBS, Cardiothoracic Surgical Unit, Royal Prince Alfred Hospital, Missenden Rd, Camperdown, New South Wales 2050, Australia (E-mail: valsby{at}hotmail.com).

Objective: Endothelial cell dysfunction has been implicated in the inflammatory response to cardiopulmonary bypass, and the upregulation of endothelial cell expression of adhesion molecules might promote leukocyte extravasation in vivo. Soluble endothelial cell adhesion molecules are increased after bypass. The aim of this study was to investigate the relationship between endothelial cell-surface expression of adhesion molecules and their concentration in plasma after coronary artery bypass grafting.
Methods: Ten patients undergoing coronary artery bypass with cardiopulmonary bypass had 5 plasma samples taken at defined intervals before, during, and after cardiopulmonary bypass. Plasma was incubated with human umbilical vein endothelial cell monolayers, and expression of E-selectin, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 on the surface of human umbilical vein endothelial cell monolayers was measured by means of enzyme-linked immunosorbent assay. Plasma soluble adhesion molecules, C-reactive protein, interleukin 8, interleukin 10, transforming growth factor ß1, and neutrophil counts were determined for each patient.
Results: Markers typical of acute inflammation (ie, interleukin 8, neutrophils, and C-reactive protein) were all increased after bypass. Soluble plasma intercellular and vascular cell adhesion molecule 1 (but not E-selectin) were increased after bypass. However, endothelial cell expression of vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 (but not E-selectin) were significantly decreased by exposure to postbypass plasma. Additionally, postbypass plasma inhibited interleukin 1ß-stimulated endothelial cell expression of vascular cell and intercellular adhesion molecule 1. Interleukin 10 and transforming growth factor ß1, both of which are known to inhibit endothelial cell adhesion molecule expression, were respectively increased 10-fold and 3-fold (P < .05) after bypass.
Conclusions: Despite containing increased soluble intercellular and vascular cell adhesion molecule 1, postbypass plasma inhibits endothelial cell expression of intercellular and vascular cell adhesion molecule 1. Upregulated vascular expression of adhesion molecules might not be essential for endothelial activation after bypass.




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