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subarachnoid hemorrhage/zea mays
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17beta-estradiol inhibits endothelin-1 production and attenuates cerebral vasospasm after experimental subarachnoid hemorrhage.
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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
Attenuation of subarachnoid hemorrhage-induced apoptotic cell death with 17 beta-estradiol. Laboratory investigation.
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OBJECTIVE
Apoptosis is implicated in vasospasm and long-term sequelae of subarachnoid hemorrhage (SAH). The authors observed that 17beta-estradiol (E2) can attenuate cerebral vasospasm, lower endothelin-1 production, and preserve normal endothelial nitric oxide synthase expression by reduction of
Upregulation of estrogen receptor alpha and mediation of 17beta-estradiol vasoprotective effects via estrogen receptor alpha in basilar arteries in rats after experimental subarachnoid hemorrhage.
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OBJECTIVE
The authors previously demonstrated that 17beta-estradiol benzoate (E2) treatment prevents subarachnoid hemorrhage (SAH)-induced cerebral vasospasm and preserves endothelial nitric oxide synthase (eNOS) in male rats. Changes in the expression of estrogen receptor (ER) subtypes ERalpha and
The effect of 17beta-estradiol in attenuating experimental subarachnoid hemorrhage-induced cerebral vasospasm.
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OBJECTIVE
Sex differences in the outcome of aneurysmal subarachnoid hemorrhage (SAH) are controversial, and the potential influence of estradiol on vasodilation is unclear. In the present study the authors evaluate the effect and possible mechanism of 17beta-estradiol (E2) on SAH-induced vasospasm
17beta-Estradiol inhibits subarachnoid hemorrhage-induced inducible nitric oxide synthase gene expression by interfering with the nuclear factor kappa B transactivation.
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OBJECTIVE
Previously, we showed that 17beta-estradiol (E(2)) treatment prevented the subarachnoid hemorrhage (SAH)-induced cerebral vasospasm in male rats. The aim of this study was designed to further delineate the molecular mechanisms underlying E(2)-induced inhibition of inducible nitric oxide
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