INTERCELLULAR ADHESION MOLECULE-1 (ICAM-1) EXPRESSION BY ENDOTHELIAL
CELLS AND SOLUBLE ICAM-1 LEVELS DO NOT CORRELATE DURING CARDIOPULMONARY
BYPASS. M. Vallely*1,2, PG. Bannon2,
CF. Hughes2, RT. Dean1, L. Kritharides1,3. The Heart Research Institute, Sydney1,
Cardiothoracic Surgical Unit, Royal Price Alfred Hospital, Sydney2,
and Department of Cardiology, Concord Hospital, Sydney3, Australia. During inflammation, there is increased adhesion to, and penetration
of, endothelium by leucocytes, and this process is dependent upon
EC expression of adhesion molecules such as ICAM-1. Cardipulmonary
bypass (CPB) causes a systemic inflammatory response syndrome which
is associated with increased levels of soluble ICAM-1 (sICAM-1).
It has hitherto been assumed that elevation of sICAM-1, implies
upregulated tissue expression of ICAM‑-1 (tICAM-1) by EC,
and that this mediates the CPB inflammatory response. The
relationship between endothelial cell (EC) expression of tICAM-1
and plasma sICAM-1 in CPB is unknown. Plasma was taken from 10 adult patients undergoing first time,
elective coronary artery bypass grafting. Samples were taken
for each patient before CPB, during CPB (before and after release
of aortic cross clamp), and 3 and 24 hours after operation (post-op).
sICAM-1 levels were measured by ELISA. The same plasma
samples were incubated with passage 2 human umbilical vein EC (HUVEC)
monolayers and cell surface expression of tICAM‑-1 measured
by ELISA. All plasma samples were corrected for haemodilution.
Each plasma sample was analysed in triplicate and all cell culture
data were mean±SD of triplicate cultures. sICAM-1 was increased in plasma 24 hours post-op (117% of pre‑-CPB;
p=0.019), but all other samples contained identical sICAM‑-1
to the pre‑-CPB control. Remarkably, HUVEC expression
of tICAM-1 was decreased by plasma sampled 3 hours post-op (85%
of control; p=0.008) and was not upregulated by any plasma sample. We conclude that plasma sICAM-1 levels are elevated late post-op,
the HUVEC expression of tICAM-1 is decreased by exposure to early
post-op blood, and the EC expression of tICAM-1 and plasma sICAM-1
need not correlate during CPB. The pro-inflammatory syndrome
of CPB may not be mediated by upregulation of EC expression of tICAM-1.
