Experimental Biology and Medicine > Volume 231, Number 6 > Pp. 1054-1057

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CENTRAL NERVOUS SYSTEM

17β-Estradiol Inhibits Endothelin-1 Production and Attenuates Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage

Chih-Lung Lin*, Aaron S. Dumont, Shu-Chuan Wu*, Chih-Jen Wang*, Sheng-Long Howng*, Yan-Fen Huang*, Wee-Yen Wong*, Neal F. Kassell, Arco Y. Jeng and Aij-Lie Kwan*1

^* Department of Neurosurgery, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan; Department of Neurosurgery, University of Virginia, Charlottesville, Virginia 22903; and Novartis Institutes for BioMedical Research, East Hanover, New Jersey 07936

¹ Department of Neurosurgery, Kaohsiung Medical University Hospital, No. 100, Tzyou 1st Road, Kaohsiung, Taiwan, Republic of China. E-mail: a_lkwan{at}yahoo.com

Though cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) has been recognized for over half a century, it remains a major complication in patients with SAH. Clinical studies have shown that elevated levels of endothelin-1 (ET-1) are present in the cerebrospinal fluid of patients with SAH, suggesting that ET-1–mediated vasoconstriction contributes to vascular constriction after SAH. Administration of estrogen promotes vasodilation in humans and in experimental animals, in part by decreasing the production of ET-1. This study evaluated the influence of 17β-estradiol (E2) on the production of ET-1 and cerebrovasospasm in an experimental SAH 2-hemorrhage model in rat. A 30-mm Silastic tube filled with E2 in corn oil (0.3 mg/ml) was subcutaneously implanted in male rats just before SAH induction. The degree of vasospasm was determined by averaging the cross-sectional areas of basilar artery 7 days after first SAH. Plasma samples collected before death were assayed for ET-1. The protective effect of E2 in attenuating vasospasm achieved statistical significance when compared with the SAH only or SAH plus vehicle groups (P < 0.01). Concentrations of ET-1 were higher in the SAH only and SAH plus vehicle groups than in controls (P < 0.001). Serum levels of ET-1 in the SAH plus E2 and E2 only groups were significantly lower than those in the SAH only and SAH plus vehicle groups (P < 0.001). There was no significant difference between ET-1 levels in the healthy control and SAH plus E2 groups. A significant correlation was found between the cross-sectional areas of basilar artery and ET-1 levels (P < 0.001). The beneficial effect of E2 in attenuating SAH-induced vasospasm may be due in part to decreasing ET-1 production after SAH. The role of E2 in the treatment of cerebral vasospasm after SAH is promising and is worthy of further investigation.

Keywords: estrogen, subarachnoid hemorrhage, vasospasm, endothelin-1

This work was supported by The National Science Council, ROC, under grant NSC91-2314-B-037-309.

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