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Vascular adhesion molecules and immunogenicity in blood vessels used as coronary artery bypass grafts

A H Chester1, J A Borland, P M Taylor

  • 1Department of Cardiothoracic Surgery, Imperial College of Science, Technology and Medicine, National Heart and Lung Institute, Harefield Hospital, Middlesex, UK.

Insights

Bypass graft vessels express molecules that attract blood cells, potentially impacting graft performance. Understanding these molecules may help improve interactions and graft outcomes.

Area of Science:

  • Vascular Biology
  • Immunology
  • Surgical Research

Background:

  • Coronary bypass graft performance is influenced by circulating cells adhering to the endothelium.
  • Cellular adherence is the first step in biological effects, preceding migration into the perivascular space.

Purpose of the Study:

  • To investigate the expression of cell adhesion molecules in human blood vessels used as bypass conduits.
  • To identify molecules regulating cell adhesion in saphenous vein, internal mammary artery, gastroepiploic artery, and inferior epigastric artery.

Main Methods:

  • Segments of four human vessel types were analyzed using monoclonal antibodies.
  • Staining targeted endothelial markers (EN-4, Pal-E, von Willebrand factor [vWF]), cell adhesion molecules (PECAM, ICAM-1, VCAM-1, E-selectin), leukocyte marker (CD45), and MHC class I and II antigens.
  • Immunoperoxidase staining visualized antigen expression.

Main Results:

  • All vessels strongly expressed endothelial markers (EN4, vWF, PECAM) and MHC class I.
  • Expression of Pal-E, ICAM-1, E-Selectin, and MHC class II (DR) was lower.
  • VCAM-1 and other MHC class II determinants (DP, DQ) showed weaker expression.
  • No significant differences in molecule expression were observed among the four vessel types.

Conclusions:

  • Vessels used for bypass grafts are immunogenic and can interact with blood components.
  • Identifying specific adhesion molecules offers potential targets for modulating these interactions and improving graft function.
Abstract

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