Taipei Medical University Institutional Repository:Item 987654321/409
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    题名: Physiological Concentration of 17β-Estradiol on Sympathetic Reinnervation in Ovariectomized Infarcted Rats.
    作者: 張念中
    Lee Tsung-Ming;Lin Mei-Shu;Chang Nen-Chung
    贡献者: 醫學系內科學科
    日期: 2008
    上传时间: 2009-08-11 13:50:32 (UTC+8)
    摘要: 17-Estradiol (E2) has been shown to exert antiarrhythmic
    effect after myocardial infarction; however, the mechanisms
    remain unclear. This study was performed to determine
    whether E2 exerts beneficial effects through attenuated sympathetic
    hyperreinnervation after infarction. Two weeks after
    ovariectomy, female Wistar rats were assigned to coronary
    artery ligation or sham operation. Twenty-four hours after
    coronary ligation, rats underwent one of five treatments: 1) sc
    vehicle treatment (control), 2) sc E2 treatment, 3) sc E2 treatment
     tamoxifen (a potent estrogen receptor antagonist), 4)
    bosentan (an endothelin receptor blocker), or 5) sc E2 treatment
     bosentan and followed for 4 wk. Myocardial endothelin-
    1 and norepinephrine levels at the remote zone revealed a
    significant elevation in control infarcted rats, compared with
    sham-operated rats, which is consistent with sympathetic hyperinnervation
    after infarction. Sympathetic hyperinnervation
    was blunted after giving the rats either E2 or bosentan,
    assessed by immunohistochemical analysis of tyrosine hydroxylase,
    growth-associated protein 43 and neurofilament,
    and Western blotting and real-time quantitative RT-PCR of
    nerve growth factor. Arrhythmic scores during programmed
    stimulation in E2-treated infarcted rats were significantly
    lower than in control-infarcted rats. Addition of bosentan did
    not have additional beneficial effects, compared with rats
    treated with E2 alone. The beneficial effect of E2 on sympathetic
    hyperinnervation was abolished by tamoxifen. Our
    data indicated that E2 has a role for sympathetic hyperinnervation
    after infarction, probably through an endothelin-1-depedent
    pathway. Chronic administration of E2 after infarction
    may attenuate the arrhythmogenic response to
    programmed electrical stimulation.
    關聯: Endocrinology.149(3):1205-1213.
    数据类型: article
    显示于类别:[內科學科] 期刊論文

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