Chapter 14. Homeometric Autoregulation

  1. Ruth Porter and
  2. David W. Fitzsimons
  1. R. G. Monroe,
  2. W. J. Gamble,
  3. C. G. Lafarge and
  4. S. F. Vatner

Published Online: 30 MAY 2008

DOI: 10.1002/9780470720066.ch14

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

Monroe, R. G., Gamble, W. J., Lafarge, C. G. and Vatner, S. F. (1974) Homeometric Autoregulation, 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.ch14

Author Information

  1. Department of Pediatrics, Harvard Medical School, and The Cardiology Department, Children's Hospital Medical Center, Boston, Massachusetts

Publication History

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

ISBN Information

Print ISBN: 9789021940250

Online ISBN: 9780470720066



  • inotropic changes;
  • unanaesthetized animals;
  • homeometric autoregulation;
  • bowditch effect;
  • starling's recovery hypothesis


The term homeometric autoregulation has been used to characterize an intrinsic mechanism which allows heart muscle to adapt to changes both in heart rate (Bowditch effect) and in developed pressure (Anrep effect). Evidence is presented that the Bowditch effect is a truly adaptive mechanism, having been observed in preparations ranging from isolated cardiac muscle strips to intact unanaesthetized animals. Recent data, however, suggest that the Anrep effect is not an intrinsic adaptive mechanism: it appears more likely that it manifests the recovery of the ventricle from transient subendocardial ischaemia induced by an abrupt increase in ventricular pressure. The resulting decrease in contractility is subsequently corrected by vascular autoregulation of the coronary bed with a redistribution of coronary flow to the ischaemic areas. Recent studies of regional coronary flow, reactive hyperaemia, the intracavitary electrocardiogram, as well as subendocardial tissue pO2 in isolated hearts and intact unanaesthetized animals confirm this.

These studies imply that, after an abrupt increase in systolic pressure, the ventricle is in a transient state of ‘decompensation’ owing to temporary subendocardial ischaemia corrected immediately by a redistribution of coronary blood to the ischaemic areas. The decompensation is, presumably, more severe in disease states such as caronary insufficiency and left ventricular hypertension, and could under such circumstances lead to serious arrhythmias. The proposed mechanism also suggests that coronary vasodilatation is accompanied by positive inotropism in the normal heart.