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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.
Insights
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.
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.
Abstract:
Coronary arterial inflow is impeded and venous outflow is increased as a result of the decrease in coronary vascular volume due to cardiac contraction. We evaluated whether cardiac contraction is influenced by interfering with the changes of the coronary vascular volume over the heart cycle. Length-tension relationships were determined in Tyrode-perfused rat papillary muscle and when coronary vascular volume changes were partly inhibited by filling it with congealed gelatin or perfusing it with a high viscosity dextran buffer. Also, myocyte thickening during contraction was reduced by placing a silicon tube around the muscle. Increasing perfusion pressure from 8 to 80 cmH2O, increased developed tension by approximately 40%. When compared with the low perfusion state, developed tension of the gelatin-filled vasculature was reduced to 43 +/- 6% at the muscle length where the muscle generates the largest developed tension (n = 5, means +/- SE). Dextran reduced developed tension to 73 +/- 6% (n = 6). The silicon tube, in low perfusion state, reduced the developed tension to 83 +/- 7% (n = 4) of control. Time-control and oxygen-lowering experiments show that the findings are based on mechanical effects. Thus interventions to prevent myocyte thickening reduce developed tension. We hypothesize that when myocyte thickening is prevented, intracellular pressure increases and counteracts the force produced by the contractile apparatus. We conclude that emptying of the coronary vasculature serves a physiological purpose by facilitating cardiomyocyte thickening thereby augmenting force development.