Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/1839
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 18034/20233 (89%)
Visitors : 23369779      Online Users : 517
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/1839


    Title: 鉛導致血壓改變的機轉探討-交感神經方面的研究
    The Change of Blood Pressure in Lead Poisoning and Its Mechanism: Study of Sympathetic Nervous System
    Authors: 張慧柔
    Huoy-Ro Chang
    Contributors: 化妝品應用與管理系
    Keywords: 
    交感神經系統
    腎上腺素接受器
    兒茶酚胺
    血壓
    Lead
    Sympathetic nervous system
    Adrenergic receptor
    Catecholamine
    Blood pressure
    Date: 1998
    Issue Date: 2008-07-18 16:08:16 (UTC+8)
    Publisher: 台南縣:嘉南藥理科技大學化妝品應用與管理系
    Abstract: 鉛會導致高血壓,並且會造成交感神經系統失調。然而,在交感神經系統對血壓的影響方面,心臟、血管和腎臟的.beta.腎上腺受體,血管的.alpha.腎上腺受體,以及血中兒茶酚胺濃度的改變扮演著重要角色。研究對象為Vistar大白鼠,我們慢性餵其不同濃度(2%,1%,0.5%,0.1%,0.05%,0.01%,0%)的醋酸鉛二個月後,測其血壓、血中兒茶酚胺濃度、血中鉛含量、血中ZPP值、心臟、血管和腎臟的.beta.腎上腺受體密度和親合力,以及血管的.alpha.腎上腺受體密度和親合力。結果顯示隨著鉛暴露量的增加,血壓、血中兒茶酚胺濃度、血中鉛含量、血中ZPP值以及腎臟的.beta.腎上腺受體密度有明顯的增加,但是心臟和血管的.beta.腎上腺受體密度有明顯的降低,然而心臟、血管和腎臟的.beta.腎上腺受體親合力則沒有任何變化。結論,從交感神經對血壓調節的機制,我們認為鉛造成血中兒茶酚胺濃度的增加、血管.beta.腎上腺受體密度的降低以及腎臟.beta.腎上腺受體密度的增加,可能是導致血壓增加的原因。另外在鉛造成的心肌收縮力的降低,可能與心臟的.beta.腎上腺受體密度的減少有非常密切的關係。
    Relation: 計畫編號:NSC87-2314-B041-013
    Appears in Collections:[Dept. of Cosmetic Science and institute of cosmetic science] MOST Project

    Files in This Item:

    File Description SizeFormat
    NSC87-2314-B041-013.pdf285KbAdobe PDF563View/Open


    All items in CNU IR are protected by copyright, with all rights reserved.


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback