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1 Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Midicinal Research Laboratories, Taisho Pharmaceutical Co. Ltd, Saitama, Saitama, Japan
3 Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: rroman{at}mcw.edu.
Recent studies have indicated that 20-hydroxyeicosatetraenoic acid (20-HETE) contributes to the fall in cerebral blood flow (CBF) following subarachnoid hemorrhage (SAH) but the factors that stimulate the production of 20-HETE are unknown. This study examines the role of vasoactive factors released by clotting blood versus the scavenging of NO by hemogloblin (Hb) in the fall in CBF following SAH. Intracisternal (icv) injection of blood produced a greater and more prolonged (120 versus 30 min) decrease in CBF than that produced by a 4% solution of Hb. Pretreated of rats with L-NAME (10 mg/kg, i.v.) to block the synthesis of NO had no effect on the fall in CBF produce by an icv injection of blood. L-NAME enhanced rats than attenuated the fall in CBF produced by an icv injection of Hb. Blockade of the synthesis of 20-HETE with TS-011 (0.1 mg/kg, i.v.) prevented the sustained fall in CBF produced by an icv injection of blood and the transient vasoconstrictor response to Hb. Hb (0.1%) reduced the diameter of the basilar artery (BA) of rats in vitro by 10 ± 2%. This response was reversed by TS-011 (100 nM). Pretreatment of vessels with L-NAME (300 µM) reduced the diameter of BA and blocked the subsequent vasoconstrictor response to addition of Hb to the bath. TS-011 returned the diameter of vessels exposed to L-NAME and Hb to control. These results suggest that the fall in CBF following SAH is largely due the release of vasoactive factors by clotting blood rather than the scavenging of NO by Hb and that 20-HETE contributes the vasoconstrictor response of cerebral vessels to both Hb and blood.
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