文化大學機構典藏 CCUR:Item 987654321/28468
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    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: https://irlib.pccu.edu.tw/handle/987654321/28468


    题名: 砷誘發大白鼠心律及心臟功能損害之研究
    Arsenic Induces Impairments on Cardiac Rhythm and Functions in Rats
    作者: 潘日南
    Phan, Nhut Nam
    贡献者: 生物科技研究所
    关键词: arsenic
    cardiac function
    hypertension
    ventricular hypertrophy
    日期: 2014-06
    上传时间: 2014-10-07 17:25:21 (UTC+8)
    摘要: Arsenic is a ubiquitous toxic compound that exists naturally in many sources such as soil, groundwater, and food; in which vast majority forms are Arsenite (As3+) or Arsenate (As5+). Epidemiologic studies documented that arsenic pollution caused black foot disease, cardiovascular diseases (hypertension, hypotension, cardiomyopathy), bladder cancer and skin cancer in many countries in which Taiwan was considered as high arsenic exposure country. However, the effects of arsenic at different concentration on cardiac functions still lack of investigation while some studies mainly focus on inflammatory and cancer mechanisms. In the present study, arsenic was fed orally to Sprague Dawley rats at 1ppm and 3.5ppm in concentration for four weeks and eight weeks duration. Using hemodynamic method as the main tool, the findings suggest that arsenical exposure at low concentration (1ppm) caused hypertension, increase in left ventricular systolic pressure (LVSP) and left ventricular end diastolic pressure (LVEDP), alteration in cardiac contractility index after four weeks and even more serve in eight weeks; whereas at the concentration of 3.5ppm, arsenic exposure leaded hypotension (8 weeks), decrease in LVSP and dramatically increase in LVEDP (8 weeks) which is supposed to cause sudden cardiac death. Moreover, QT prolongation, heart rate decline, widen in cardiac cycle length are also induced by arsenic in time-concentration profiles. These alterations are supposed to be the interaction between arsenic and cardiac nerves activity via the changing in calcium homeostasis. Collectively, our quantitative PCR and western blot data strongly suggest that calcium homeostasis may also go through MEF2A, TNNI3, CAMKK2, CALM3 and cardiac hypertrophy relative signaling pathway.
    显示于类别:[生物科技研究所 ] 博碩士論文

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