Mechanisms contributing to pulsus alternans in pressure-overload cardiac hypertrophy. Academic Article uri icon

Overview

abstract

  • The mechanisms underlying pulsus alternans in pressure-over-load (POL) cardiac hypertrophy were investigated. Simultaneous measurements of force and intracellular Ca2+ (using fura 2) in right ventricular papillary muscles under conditions that produced mechanical alternans, revealed alternation of the amplitude of the Ca2+ transient together with alternation of force in some POL muscles. Instances when alternation of force occurred without any apparent alternation of the Ca2+ transient were also observed. Exposure of muscles to 5 microM ryanodine significantly attenuated mechanical alternans, thereby implicating a role for the sarcoplasmic reticulum (SR) in this process. The time course of restitution of force and the intracellular Ca2+ transient were, however, unchanged in POL hearts, indicating that SR Ca2+ cycling was not appreciably slowed. The fraction of Ca2+ recirculated intracellularly was derived from studies of postextrasystolic potentiation and was significantly reduced in the POL hearts, suggesting additional differences in cellular Ca2+ regulation. We conclude that changes in Ca2+ handling play an important role in the onset of mechanical alternans in POL hypertrophy, but that additional factors, most likely a slowing of crossbridge cycling rate, are also likely to be important.

publication date

  • December 1, 1996

Research

keywords

  • Cardiomegaly
  • Hypertension
  • Pulse

Identity

Scopus Document Identifier

  • 0030473032

Digital Object Identifier (DOI)

  • 10.1152/ajpheart.1996.271.6.H2490

PubMed ID

  • 8997309

Additional Document Info

volume

  • 271

issue

  • 6 Pt 2