Chapter 9. Tetanized Cardiac Muscle

  1. Ruth Porter and
  2. David W. Fitzsimons
  1. Lincoln E. Ford and
  2. Robert Forman

Published Online: 30 MAY 2008

DOI: 10.1002/9780470720066.ch9

Ciba Foundation Symposium 24 - Physiological Basis of Starling's Law of the Heart

Ciba Foundation Symposium 24 - Physiological Basis of Starling's Law of the Heart

How to Cite

Ford, L. E. and Forman, R. (1974) Tetanized Cardiac Muscle, in Ciba Foundation Symposium 24 - Physiological Basis of Starling's Law of the Heart (eds R. Porter and D. W. Fitzsimons), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470720066.ch9

Author Information

  1. Cardiovascular Division, Perer Bent Brigham Hospital, Boston, Massachusetts

Publication History

  1. Published Online: 30 MAY 2008
  2. Published Print: 1 JAN 1974

ISBN Information

Print ISBN: 9789021940250

Online ISBN: 9780470720066

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Keywords:

  • electrical stimulation;
  • length-tension curve;
  • tetanized cardiac muscle;
  • muscle length;
  • contraction cycle

Summary

We developed a method of tetanizing cat papillary muscle to determine the length dependence of the force-velocity characteristic of cardiac muscle in conditions where activation could be independent of time in the contraction cycle. The muscle was tetanized by repetitive electrical stimulation in the presence of 10mM-caffeine and an increase in calcium concentration (to 7.5–12.5 Mm). These agents appear to delay the onset of relaxation so that repetitive stimulation re-activates the muscle before relaxation begins. The force-velocity relations were measured at different muscle lengths that had been corrected for series elastic element extension. These lengths ranged from 81 to 97 % of the contractile unit length at which maximum force is produced. The data were fitted by a least-squares method with hyperbolae described by the Hill equation, each for a constant, corrected muscle length. The extrapolated maximum velocities and the isometric forces diminished together in almost direct proportion to the amount of contractile unit shortening. The results can be explained by deactivation of the contractile elements in the presence of a small internal load. The ability of the heart to dilate suggests that, under normal conditions, the ventricular muscle must operate near the short end of its physiological range and that the range of lengths studied, therefore, included all but the shortest lengths in the physiological range. Consideration of the circumferential changes that must occur in the intact heart and of the physiological characteristics of the isolated muscle suggest that the Starling phenomenon results, in part, from a recruitment of endocardial layers of muscle and from a proportionately greater increase in the work of these inner layers as the heart dilates.