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Decrease in coronary vascular volume in systole augments cardiac contraction.

M J Willemsen1, D J Duncker, R Krams

  • 1Laboratory for Physiology, Institute for Cardiovascular Research, Vrije Universiteit, 1081 BT Amsterdam, The Netherlands.

American Journal of Physiology. Heart and Circulatory Physiology
|July 17, 2001
PubMed
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Cardiac contraction reduces coronary vascular volume, impacting heart muscle force. Inhibiting this volume change impairs cardiomyocyte thickening and reduces developed tension, suggesting a physiological role for vascular emptying in augmenting heart force.

Area of Science:

  • Cardiovascular Physiology
  • Cardiac Mechanics

Background:

  • Cardiac contraction impedes coronary arterial inflow and increases venous outflow by decreasing coronary vascular volume.
  • The functional significance of these dynamic changes in coronary vascular volume during the cardiac cycle remains incompletely understood.

Purpose of the Study:

  • To investigate whether altering the normal changes in coronary vascular volume during the cardiac cycle influences cardiac contraction.
  • To determine the mechanical consequences of inhibiting coronary vascular volume changes on myocardial contractility.

Main Methods:

  • Utilized Tyrode-perfused rat papillary muscle preparations.
  • Interfered with coronary vascular volume changes by filling vasculature with gelatin or perfusing with high-viscosity dextran buffer.
  • Reduced myocyte thickening during contraction by applying a constrictive silicon tube.

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Main Results:

  • Increasing perfusion pressure significantly increased developed tension.
  • Gelatin filling of the vasculature reduced developed tension to 43% of control at optimal muscle length.
  • High-viscosity dextran and external constriction by a silicon tube also significantly reduced developed tension.
  • Mechanical effects, not altered oxygen levels, were responsible for the observed reductions in force.

Conclusions:

  • Interventions that prevent or reduce cardiomyocyte thickening during contraction lead to a decrease in developed tension.
  • It is hypothesized that preventing myocyte thickening increases intracellular pressure, counteracting the force generated by the contractile apparatus.
  • The emptying of the coronary vasculature during systole likely serves a physiological purpose by facilitating cardiomyocyte thickening and thereby augmenting cardiac force development.