关键词: 雌二醇; 蛛网膜下腔出血; 血管痉挛; 颅内

Abstract: Objective Although cerebral vasospasm after aneurismal subarachnoid hemorrhage (SAH) hasbeen recognized for over half of a century, it remains a major complication in patients sufferingfrom SAH. As the problem of no effective treatment for cerebral vasospasm still exists, thepathophysiological mechanism contributing to arterial dysfunction needs intensive study. Thepresent study evaluates the effect and possible mechanism of 17β-estradiol (E2) on SAH-inducedvasospasm in a two-hemorrhage rodent model of SAH.Methods A 30-mm Silastic® tube filled with E2 in corn oil (0.3 mg/ml) was subcutaneouslyimplanted in male rats. Serum levels of E2 were measured on day 0, 1, 2, 3, 4, and 7 afterimplantation. The degree of vasospasm was determined by averaging the cross sectional areasof the basilar artery 7 days after the first SAH. Expressions of endothelial nitric oxide synthase(eNOS) and inducible nitric oxide synthase (iNOS) in basilar artery were also evaluated.Results Serum levels of E2 in the E2-treated rats were at physiological levels (56-92 pg/ml) andwere significantly higher than those in the control and vehicle groups. E2-treatment significantly(P <0.01) attenuated SAH-induced vasospasm. Induction of iNOS-mRNA and protein in basilarartery by SAH was significantly diminished by E2-treatment but not by vehicle. The SAHinducedsuppression of eNOS-mRNA and protein was relieved by E2 treatment.Conclusion These results suggest that continuous treatment of E2 at physiological level preventscerebral vasospasm following SAH. The beneficial effect of E2 may be, in part, related to prevent the augmentation of iNOS expression and preserve the normal eNOS expression after SAH. E2-treatment holds therapeutic promise in the treatment of cerebral vasospasm following SAH and ismeritorious of further investigation.

Key words: Estradiol; Subarachnoid hemorrhage; Vasospam intracramial