© 1997 American Heart Association, Inc.
Articles |
Induction of Cyclooxygenase-2 in Human Saphenous Vein and Internal Mammary Artery
From the Department of Applied Pharmacology (D.B.-B., S.W.L.) and Department of Thoracic Medicine (E.-B.H., R.N.), National Heart and Lung Institute, Imperial College of Science, Technology and Medicine; and Department of Cardiothoracic Surgery (J.R.P.) and Department of Anaesthetics and Critical Care Medicine (J.A.M.), Royal Brompton National Heart and Lung Hospital, London, UK.
Correspondence to Dr Jane A. Mitchell, Department of Anaesthetics and Critical Care Medicine, Royal Brompton National Heart and Lung Hospital, Sydney Street, London SW3 6NP, UK.
Abstract Within vessels, cyclooxygenase
(COX) is expressed constitutively (COX-1) in
endothelial cells where its production of
prostacyclin is thought to contribute to the maintenance of
vascular integrity. Recently, a novel isoform of COX, COX-2, has been
described that is induced in animal arterial vessels after
physical damage or exposure to proinflammatory cytokines.
However, induction of COX-2 in human vessels has not been
characterized. Moreover, the relative ability of arteries and veins to
express COX-2 has not been addressed. Thus, we have compared the
ability of segments of human saphenous vein and internal mammary
artery, obtained from the same patient, to express COX-2 activity and
mRNA after organ culture in the presence and absence of
interleukin-1ß. COX-2 metabolites, measured by radioimmunoassay, were
released by both the internal mammary artery and saphenous vein in the
following rank order: prostaglandin
E2
prostacyclin thromboxane
A2. Inclusion of interleukin-1ß in the culture medium
increased the release of prostanoids by the saphenous vein but not by
the internal mammary artery. However, the selective COX-2
inhibitor NS-398 significantly attenuated prostacyclin
release from both tissues. Northern blot analysis showed no
detectable COX-2 mRNA in freshly prepared saphenous vein or internal
mammary artery. In contrast, after 48 hours in organ culture, low
levels of COX-2 mRNA were detected in both internal mammary artery and
saphenous vein, an effect that was greatly increased by
interleukin-1ß. These observations show that COX-2 is induced in
human saphenous vein and internal mammary artery and suggest that this
may occur in humans after coronary artery bypass graft surgery.
The induction of COX-2 and subsequent release of prostacyclin may
represent an endogenous defense mechanism against
endothelial damage incurred during surgical preparation
of these vessels for bypass.
Key Words: cyclooxygenase • saphenous vein • internal mammary artery • prostacyclin
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