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(Stroke. 1998;29:683-689.)
© 1998 American Heart Association, Inc.

Original Contributions

Effect of Vasospasm on Heme Oxygenases in a Rat Model of Subarachnoid Hemorrhage

Minoru Kuroki, MD; Kenji Kanamaru, MD, DMSc; Hidenori Suzuki, MD; Shiro Waga, MD, DMSc; Reiji Semba, MD, PhD

From the Departments of Neurosurgery (M.K., K.K., H.S., S.W.) and Anatomy II (R.S.), Mie University School of Medicine, Mie, Japan.

Correspondence to: Kenji Kanamaru, MD, DMSc, Department of Neurosurgery, Mie University School of Medicine, Tsu, Mie 514, Japan. E-mail kanamaru{at}clin.medic.mie-u.ac.jp

Background and Purpose—Subarachnoid hemorrhage (SAH)-induced heme oxygenase-1 (HO-1) in glia throughout the rat brain without affecting heme oxygenase-2 (HO-2). However, the relationship between cerebral vasospasm and the expression of heme oxygenases after SAH is thus far unknown. The purpose of the present study was to clarify the effect of vasospasm on the expression of heme oxygenases in a rat model of SAH.

Methods—Endothelin, hemolysate, hemolysate saturated with carbon monoxide (CO-hemolysate), and saline were injected into the cisterna magna of adult rats. Angiography was repeated before each injection and 15 and 60 minutes and 24 hours after each injection. Immunocytochemistry for HO-1, HO-2, and glial fibrillary acidic protein (GFAP) was performed 24 hours after the injection.

Results—A significant vasospasm occurred in the basilar artery after the injection of endothelin, hemolysate, and CO-hemolysate. The degree of vasospasm was most prominent 15 minutes after each injection. There was no significant difference in the degree of vasospasm among injections. The HO-1 was induced exclusively in the glial cells throughout the brain after injection of hemolysate and CO-hemolysate; however, it was not induced by endothelin and saline. In the dentate gyrus of the hippocampus and the molecular layer of the cerebellum, the HO-1-positive cells were also stained for GFAP, suggesting astrocytic glial cells. On the other hand, HO-2 immunoreactivity was abundant in neurons and was not affected by endothelin, hemolysate, CO-hemolysate, or saline.

Conclusions—It is suggested that heme per se, rather than ischemia induced by vasospasm, plays a pivotal role in the expression of HO-1 in this rat model.

Editorial Comment

Frank R. Sharp, MD, Guest Editor

Departments of Neurology and Neurosurgery, University of California at San Francisco, VA Medical Center, San Francisco, California

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