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Vol. 300, Issue 2, 393-398, February 2002
Departments of Clinical Pharmacology and Surgery, and Institute of
Biopharmaceutical Sciences, Royal College of Surgeons in Ireland,
Dublin, Ireland
Prostaglandin formation is enhanced in vascular disease, in part
through induction of cyclooxygenase (COX-2) in vascular smooth muscle
cells. Because COX regulates cell growth and migration, we examined
whether the COX expression plays a role in the development of intimal
hyperplasia after vascular injury. Rats undergoing balloon angioplasty
of the carotid artery were randomized to receive a selective COX-2
inhibitor (SC-236), a selective COX-1 inhibitor (SC-560) or a
combination of the two. Normal, uninjured vessels showed COX-1, but no
COX-2 expression. Fourteen days after balloon injury, both COX-1 and
COX-2 were expressed in the neointima. Balloon angioplasty resulted in
a marked increase in the urinary excretion of prostaglandin (PG)
E2, PGF2
, and thromboxane (TX)
B2. Both the COX-1 inhibitor SC-560 and the COX-2 inhibitor SC-236 suppressed the generation of PGE2 and
PGF2, particularly when combined, suggesting a role for
both isozymes in the generation of prostaglandins in this model. In
contrast, TXA2 was markedly suppressed by the COX-1
inhibitor SC-560. COX-2 inhibition with SC-236 had no effect on intimal
hyperplasia at day 14 (0 versus 8.5%; n = 7 in
controls). In contrast, intimal hyperplasia was reduced by SC-560 when
administered alone (by 42%; n = 7, p < 0.05) or in combination with SC-236 (by 40%;
n = 7, p < 0.05). COX-1 may
play a role in the development of intimal hyperplasia, potentially
through the inhibition of platelet TXA2. Despite being expressed in the neointima, COX-2 does not play a role in the development of intimal hyperplasia after vascular injury.
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