Decrease in coronary vascular volume in systole augments cardiac contraction

Willemsen, Mark G. A.; Duncker, Dirk J.; Krams, Rob; Dijkman, Marieke A.; Lamberts, Regis R.; Sipkema, Pieter; Westerhof, Nico

doi:10.1152/ajpheart.2001.281.2.h731

Cited by 14 publications

(12 citation statements)

References 25 publications

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“…This concept is formulated by the varying elastance model. An increase in stiffness of the cardiac muscle (vessel environment) decreases vessel lumen similar to what happens in the ventricular lumen during contraction (245,387,447); in the muscle shortening and thickening model, the shortening and related thickening of the muscle fibers during contraction cause a decrease in vessel diameters (426,450); and in the vascular deformation model, deformation of the vasculature, vessel shortening, changes in bifurcation angles, and changes in tortuosity result from muscle contraction (169).…”

Section: Models Explaining the Diastolic-systolic Changes Of The Vmentioning

confidence: 98%

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Westerhof¹,

Boer²,

Lamberts³

et al. 2006

Physiological Reviews

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231

209

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The cardiac muscle and the coronary vasculature are in close proximity to each other, and a two-way interaction, called cross-talk, exists. Here we focus on the mechanical aspects of cross-talk including the role of the extracellular matrix. Cardiac muscle affects the coronary vasculature. In diastole, the effect of the cardiac muscle on the coronary vasculature depends on the (changes in) muscle length but appears to be small. In systole, coronary artery inflow is impeded, or even reversed, and venous outflow is augmented. These systolic effects are explained by two mechanisms. The waterfall model and the intramyocardial pump model are based on an intramyocardial pressure, assumed to be proportional to ventricular pressure. They explain the global effects of contraction on coronary flow and the effects of contraction in the layers of the heart wall. The varying elastance model, the muscle shortening and thickening model, and the vascular deformation model are based on direct contact between muscles and vessels. They predict global effects as well as differences on flow in layers and flow heterogeneity due to contraction. The relative contributions of these two mechanisms depend on the wall layer (epi- or endocardial) and type of contraction (isovolumic or shortening). Intramyocardial pressure results from (local) muscle contraction and to what extent the interstitial cavity contracts isovolumically. This explains why small arterioles and venules do not collapse in systole. Coronary vasculature affects the cardiac muscle. In diastole, at physiological ventricular volumes, an increase in coronary perfusion pressure increases ventricular stiffness, but the effect is small. In systole, there are two mechanisms by which coronary perfusion affects cardiac contractility. Increased perfusion pressure increases microvascular volume, thereby opening stretch-activated ion channels, resulting in an increased intracellular Ca2+ transient, which is followed by an increase in Ca2+ sensitivity and higher muscle contractility (Gregg effect). Thickening of the shortening cardiac muscle takes place at the expense of the vascular volume, which causes build-up of intracellular pressure. The intracellular pressure counteracts the tension generated by the contractile apparatus, leading to lower net force. Therefore, cardiac muscle contraction is augmented when vascular emptying is facilitated. During autoregulation, the microvasculature is protected against volume changes, and the Gregg effect is negligible. However, the effect is present in the right ventricle, as well as in pathological conditions with ineffective autoregulation. The beneficial effect of vascular emptying may be reduced in the presence of a stenosis. Thus cardiac contraction affects vascular diameters thereby reducing coronary inflow and enhancing venous outflow. Emptying of the vasculature, however, enhances muscle contraction. The extracellular matrix exerts its effect mainly on cardiac properties rather than on the cross-talk between cardiac muscle and coronary c...

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Section: Models Explaining the Diastolic-systolic Changes Of The Vmentioning

confidence: 98%

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Westerhof¹,

Boer²,

Lamberts³

et al. 2006

Physiological Reviews

Self Cite

231

209

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“…7) (79, 331, 399, 400, 481). Additional hypotheses to explain the coronary effects of myocardial contraction include recognition of variations in myocardial stiffness during the cardiac cycle (varying elastance model) (583–585), increases in cardiomyocyte diameter during isotonic cardiac contractions (muscle shortening and thickening model) (977), as well as changes in the shape of vascular cross-sections, branching angles, vessel tortuosity (vascular deformation model) (342, 770). As with any physiologic system, it is likely that the true origins and regulation of phasic coronary flow are the result of multiple processes which can only be truly modeled by integrating multiple hypotheses.…”

Section: Extravascular Compression and Transmural Flow Distributionmentioning

confidence: 99%

Regulation of Coronary Blood Flow

Goodwill

Dick

Kiel

et al. 2017

Comprehensive Physiology

234

248

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The heart is uniquely responsible for providing its own blood supply through the coronary circulation. Regulation of coronary blood flow is quite complex and, after over 100 years of dedicated research, is understood to be dictated through multiple mechanisms that include extravascular compressive forces (tissue pressure), coronary perfusion pressure, myogenic, local metabolic, endothelial as well as neural and hormonal influences. While each of these determinants can have profound influence over myocardial perfusion, largely through effects on end-effector ion channels, these mechanisms collectively modulate coronary vascular resistance and act to ensure that the myocardial requirements for oxygen and substrates are adequately provided by the coronary circulation. The purpose of this series of Comprehensive Physiology is to highlight current knowledge regarding the physiologic regulation of coronary blood flow, with emphasis on functional anatomy and the interplay between the physical and biological determinants of myocardial oxygen delivery.

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“…In case of uncertainty in reported parameters, sensitivity analysis was performed to examine the robustness of the study conclusions to these parameters. These include the degree of transmission of shortening-induced intramyocyte pressure (48,72) to neighboring vessels as represented by the proportionality parameter ␣ in Eqs. 2b and 2e, which was varied between zero and three times its baseline value.…”

Section: Sensitivity and Robustness Analysismentioning

confidence: 99%

“…It suggests decreased contractility under lower perfusion. The rational for this simplification is twofold: it is still controversial (71,72) if contractility is indeed reduced, and in addition, even if included, it is not expected to change the study conclusions, since all but the predictions of Fig. 5 relate to baseline perfusion and, hence, a constant contractility state.…”

Section: Critique Of the Modelmentioning

confidence: 99%

Mechanisms of myocardium-coronary vessel interaction

Algranati

Kassab

Lanir

2010

American Journal of Physiology-Heart and Circulatory Physiology

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The mechanisms by which the contracting myocardium exerts extravascular forces (intramyocardial pressure, IMP) on coronary blood vessels and by which it affects the coronary flow remain incompletely understood. Several myocardium-vessel interaction (MVI) mechanisms have been proposed, but none can account for all the major flow features. In the present study, we hypothesized that only a specific combination of MVI mechanisms can account for all observed coronary flow features. Three basic interaction mechanisms (time-varying elasticity, myocardial shortening-induced intracellular pressure, and ventricular cavity-induced extracellular pressure) and their combinations were analyzed based on physical principles (conservation of mass and force equilibrium) in a realistic data-based vascular network. Mechanical properties of both vessel wall and myocardium were coupled through stress analysis to simulate the response of vessels to internal blood pressure and external (myocardial) mechanical loading. Predictions of transmural dynamic vascular pressure, diameter, and flow velocity were determined under each MVI mechanism and compared with reported data. The results show that none of the three basic mechanisms alone can account for the measured data. Only the combined effect of the cavity-induced extracellular pressure and the shortening-induced intramyocyte pressure provides good agreement with the majority of measurements. These findings have important implications for elucidating the physical basis of IMP and for understanding coronary phasic flow and coronary artery and microcirculatory disease.

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Decrease in coronary vascular volume in systole augments cardiac contraction

Cited by 14 publications

References 25 publications

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Regulation of Coronary Blood Flow

Mechanisms of myocardium-coronary vessel interaction

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