Coronary pressure-flow relations and the vascular waterfall

Westerhof, Nico; Sipkema, Pieter; Huis, G A van

doi:10.1093/cvr/17.3.162

Cited by 19 publications

(9 citation statements)

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“…The coronary circulation provides an analogous system to study the impact of oscillating external pressures on blood flow, since myocardial contraction increases the tissue pressure around coronary blood vessels. Retrograde flow and the inverse relationship between pressure and flow oscillation amplitude predicted by our thought experiment have been documented experimentally in the coronary beds of dogs (Spaan et al, 1981) and in a hydraulic model (Westerhof et al, 1983) and a computer model (Lee et al, 1984) of the coronary circulation. In these experiments, conditions were altered by varying the magnitude of an upstream resistor, equivalent to R u .…”

Section: Waterfall Formation Can Reduce Oscillation Of Caval Flowsupporting

confidence: 55%

The caval sphincter in cetaceans and its predicted role in controlling venous flow during a dive

Lillie

Vogl

Raverty³

et al. 2018

Journal of Experimental Biology

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A sphincter on the inferior vena cava can protect the heart of a diving mammal from overload when elevated abdominal pressures increase venous return, yet sphincters are reported incompetent or absent in some cetacean species. We previously hypothesized that abdominal pressures are elevated and pulsatile in fluking cetaceans, and that collagen is deposited on the diaphragm according to pressure levels to resist deformation. Here, we tested the hypothesis that cetaceans generating high abdominal pressures need a more robust sphincter than those generating low pressures. We examined diaphragm morphology in seven cetacean and five pinniped species. All odontocetes had morphologically similar sphincters despite large differences in collagen content, and mysticetes had muscle that could modulate caval flow. These findings do not support the hypothesis that sphincter structure correlates with abdominal pressures. To understand why a sphincter is needed, we simulated the impact of oscillating abdominal pressures on caval flow. Under low abdominal pressures, simulated flow oscillated with each downstroke. Under elevated pressures, a vascular waterfall formed, greatly smoothing flow. We hypothesize that cetaceans maintain high abdominal pressures to moderate venous return and protect the heart while fluking, and use their sphincters only during low-fluking periods when abdominal pressures are low. We suggest that pinnipeds, which do not fluke, maintain low abdominal pressures. Simulations also showed that retrograde oscillations could be transmitted upstream from the cetacean abdomen and into the extradural veins, with potentially adverse repercussions for the cerebral circulation. We propose that locomotion-generated pressures have influenced multiple aspects of the cetacean vascular system.

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Section: Waterfall Formation Can Reduce Oscillation Of Caval Flowsupporting

confidence: 55%

The caval sphincter in cetaceans and its predicted role in controlling venous flow during a dive

Lillie

Vogl

Raverty³

et al. 2018

Journal of Experimental Biology

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show abstract

“…However, the compliance effects of all vessels are undeniable and of such a magnitude that these may not be neglected in model studies in which Starling resistors are incorporated. Reports trying to bridge both concepts have already been presented (Westerhof et al, 1983;Downey et al, 1983). The author's personal opinion, however, is that a Starling resistor mechanism in the autoregulated heart is not likely at other than venous levels.…”

Section: Discussionmentioning

confidence: 99%

Coronary diastolic pressure-flow relation and zero flow pressure explained on the basis of intramyocardial compliance.

Spaan¹

1985

Circulation Research

183

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In the controversy about the mechanisms determining the high zero flow pressures and the further interpretation of coronary diastolic pressure flow relations, this paper takes a stand in favor of intramyocardial compliance as the primary cause of the high zero flow pressures. An attempt has been made to estimate the compliance distribution within the coronary circulation and to show the specific effect of intramyocardial compliance on arterial and venous pressure-flow relations. Since no data are available on the distensibility of coronary arterioles and capillaries, these data were taken from studies on mesenteric vessels. Based on these data, it is shown that, depending on the transmural pressure, smooth muscle tone may either increase or decrease arteriolar compliance. A compliance distribution has been proposed based on assumed pressure, volume, and distensibility distributions. For all but the venous division of the circulation, experimental data on volume could be found in the literature. Based on this compartmental analysis, it is predicted that overall intramyocardial compliance may exceed epicardial arterial compliance by a factor 45. The literature presenting functional evidence for intramyocardial compliance effects has been reviewed. Experimental results on venous outflow during long diastoles have been analyzed. Pf = 0 coronary pressure at zero flow, is higher when measured later in diastole. It is shown that this may be explained by charging of intramyocardial compliance in the period before flow ceases. The discrepancy between results on pressure-flow relations in the fully dilated bed and autoregulated bed are related to the differences in pressure, resistance, and compliance distributions.

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“…The first one is the vascular waterfall; this model approach was studied earlier by Gregg and Eckstein (28), it was firmly established by Downey and Kirk (23), and also studied by Archie (5), Westerhof et al (71). The other mechanism is the intramyocardial pump (8,9,63,64).…”

Section: Coronary Flow Impediment In Systolementioning

confidence: 92%

Physiological hypotheses-Intramyocardial pressure. A new concept, suggestions for measurement

Westerhof

1990

Basic Res Cardiol

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Intramyocardial pressure is supposed to play a major role in systolic coronary flow impediment. Via its assumed relation with radial wall stress it is supposed to be similar to ventricular pressure at the endocardium and decreases linearly to negligible values epicardially. Many attempts to measure intramyocardial pressure have been reported in the literature with rather different results. For instance, with most of the various methods, intramyocardial pressures both higher and lower than left ventricular pressure have been obtained and intramyocardial pressures of more than 125 mm Hg have been found in low-loaded isobaric beats (negligible pressure development in systole). In this "physiological hypotheses paper" I suggest left ventricular pressure and intramyocardial pressure both to result from the varying stiffness of cardiac muscle over the heart cycle. For any intramuscular cavity a time varying pressure-volume (P-V) relation results from the changes in muscle stiffness, the so-called time varying elastance defined as E(t) = P(t)/V(t), and with maximal or systolic elastance called Emax. For a constant contractile state the time varying elastance (E(t)) is suggested to be almost independent of preload and afterload. This concept has been well established for the ventricular cavities, but is here proposed to hold for the interstitial space as well. If a cavity is subject to isovolumic conditions the pressure will be high, but when volume in systole decreases (ventricular ejection or squeezing out of interstitial fluid) pressures will be lower. Thus for constant load on the interstitial cavities, but different loads on the ventricle, left ventricular pressure will vary while intramyocardial pressure remains the same. For low-loaded isobaric beats where left ventricular pressure is minimal intramyocardial pressure will remain the same as during normal ventricular loads and isovolumic beats. Augmented contractility will increase Emax and this will increase left ventricular and intramyocardial pressure only by the same amount if loading conditions of both cavities remain the same. Both ventricular pressure and intramyocardial pressure arise from varying stiffness of cardiac muscle and intramyocardial pressure does not result from left ventricular pressure. A proportionality of left ventricular and intramyocardial pressure is therefore not to be expected. The results on intramyocardial pressure obtained by the different methods used in the literature should be re-interpreted taking this concept into account.

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Coronary pressure-flow relations and the vascular waterfall

Cited by 19 publications

References 0 publications

The caval sphincter in cetaceans and its predicted role in controlling venous flow during a dive

The caval sphincter in cetaceans and its predicted role in controlling venous flow during a dive

Coronary diastolic pressure-flow relation and zero flow pressure explained on the basis of intramyocardial compliance.

Physiological hypotheses-Intramyocardial pressure. A new concept, suggestions for measurement

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