From the Departments of Neurosurgery (K.O., Y.S., M.T., J.Y.) and
Pharmacology (Y.W.), Nagoya University School of Medicine, Nagoya, Japan.
Correspondence and reprint requests to Yoshio Suzuki, MD, Department of Neurosurgery, Nagoya University School of Medicine, 65-Tsurumai, Showa, Nagoya, 466-0065, Japan. E-mail yosu{at}med.nagoya-u.ac.jp
Background and Purpose—Inducible
cyclooxygenase (COX-2) has been found to play a
pathological role in cerebral insult. We investigated
the expression of COX-2 in the basilar artery after experimental
subarachnoid hemorrhage (SAH).
Methods—In a canine "two-hemorrhage" model of SAH,
the basilar arteries were obtained on day 2 after a cisternal injection
of autologous blood or on days 4, 6, 7, or 9 after the second
injection. Basilar arteries also were obtained 12 hours after
intracisternal injection a cytokine: interleukin (IL)-1ß
(0.03 µg), IL-6 (3 µg), or IL-8 (10 µg). Western blotting with a
polyclonal anti–COX-2 antibody was performed in these arteries.
Results—COX-2 protein was not demonstrated in the basilar artery
in control animals without SAH. However, it was expressed in the
basilar artery on days 2, 4, 6, and 7 after blood injection but not on
day 9. Intracisternal injection of IL-1ß, IL-6, or
IL-8 also induced COX-2 in the basilar artery.
Conclusions—COX-2 expression was detected in basilar
arterial tissue in both acute and chronic stages after SAH.
Elevation of inflammatory cytokines after SAH may be involved
in the induction of COX-2, which may produce sufficient quantities of
eicosanoids to affect hemodynamics after SAH.
Department
of Physiology and Pharmacology,
Bowman Gray School of Medicine,
Wake Forest University,
Winston-Salem, North Carolina
© 1998 American Heart Association, Inc.
Original Contributions
Inducible Cyclooxygenase Expression in Canine Basilar Artery After Experimental Subarachnoid Hemorrhage
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