English  |  正體中文  |  简体中文  |  Items with full text/Total items : 6024/14565 (41%)
Visitors : 13708220      Online Users : 310
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.fy.edu.tw:8080/ir/handle/987654321/9507


    Title: Analysis of mechanical restitution and post-rest potentiation in isolated rat atrium.
    Authors: Sheng-Nan Wu;Ai-Yu Shen;Tsong-Long Hwang
    Contributors: 輔英科技大學 物理治療系
    Date: 1996-09-01
    Issue Date: 2010-11-10 09:42:37 (UTC+8)
    Abstract: Mechanical restitution and post-rest potentiation in isolated rat atria were studied in order to understand the intracellular Ca2+ handling during stimulation and interbeat interval. Various agents known to affect transmembrane Ca2+ inward current or Ca2+ accumulation of the sarcoplasmic reticulum were examined. The tissues were stimulated at 1 Hz and ectopic stimuli of different preceding intervals were driven by a programmable stimulator. The relationship between the force produced by the ectopic contraction and the duration of the preceding interval was plotted to construct mechanical restitution curves. Mechanical restitution curve was well fitted to two exponential processes, i.e., an early rapid phase followed by a slowly rising phase. It is suggested that the time constant in early phase (tau 1) of mechanical restitution curve is dependent on the reactivation of transmembrane Ca2+ inward currents as well as the translocation of Ca2+ within the sarcoplasmic reticulum. However, the time constant in late phase (tau 2) involves the rate of Ca2+ influx or efflux possibly via the Na+/Ca2+ exchange mechanism. The present studies suggest that in rat myocardium, verapamil enhances the buffering capacity of the sarcoplasmic reticulum inside the cell, while isoproterenol appears to short circuit the buffering barrier of the sarcoplasmic reticulum and enhance the flow of Ca2+ into the cytosol. Ryanodine, which accelerates the Ca2+ release from the sarcoplasmic reticulum, is believed to attenuate its buffering capacity. The present analytical methods to which the mechanical restitution and the post-rest potentiation are combined would represent a good model for the study of beat-to-beat intracellular Ca2+ handling in cardiac muscle.
    Relation: Chin. J. Physiol. 39(1),23-29
    Appears in Collections:[物理治療系] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML594View/Open


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


    本網站典藏內容為學術研究目的之提供,請尊重著作權人之權益合理使用,請勿任意重製、轉貼、改作及散佈。

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