Effect of flow and vascular heterogeneity on glucose metabolism in isolated dog hearts

Kuikka, Jyrki T.

doi:10.1046/j.1365-2281.2002.00408.x

Cited by 3 publications

(2 citation statements)

References 25 publications

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“…Heterogeneity of flow is present in ischemia in the patient (344). Oxygen consumption, glucose uptake, glycolytic enzyme activity, and oxygen delivery are related and also heterogeneously distributed (6,158,179,252,372). In addition to flow heterogeneity, flow regulation (193), metabolic control of flow (98), vasomotion (400), microvascular coronary ␣-adrenergic vasoconstriction (77), and responses to drugs (78,236,265) are all heterogeneously distributed.…”

Section: A Functional Arrangement Of the Cardiac Muscle And The Coromentioning

confidence: 99%

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Westerhof¹,

Boer²,

Lamberts³

et al. 2006

Physiological Reviews

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: A Functional Arrangement Of the Cardiac Muscle And The Coromentioning

confidence: 99%

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Westerhof¹,

Boer²,

Lamberts³

et al. 2006

Physiological Reviews

231

209

View full text Add to dashboard Cite

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“…2 ) has to be taken also into account, for example, due to a possible flow dependency (13). Furthermore, the results obtained by Cousineau et al (3) in dog heart suggest that ␤-adrenergic blockade may change organ transit time dispersion, besides its effect on Q distribution (17).…”

mentioning

confidence: 99%

Cardiac output and systemic transit time dispersion as determinants of circulatory mixing time: a simulation study

Weiß¹

2009

Journal of Applied Physiology

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A new approach to characterize the kinetics of intravascular mixing process is presented. The mixing time, defined as the time required for achieving 95% homogeneity, is calculated by numerical simulations using a circulatory model applied to the intravascular marker indocyanine green (ICG). The results suggest that the mixing time is determined by cardiac output and the relative dispersion of transit time distribution across the systemic circulation, whereby the rate of mixing increases with increasing cardiac output and decreasing transit time dispersion, and vice versa. The estimation of plasma volume from simulated ICG dilution data using the backextrapolation method shows that slow mixing is accompanied by an overestimation of blood volume. This error may be negligible for mixing times of less than approximately 3 min but high in disease states characterized by low cardiac output and/or high transit time dispersion. In view of the role of transit time dispersion as determinant of intravascular mixing, it would be interesting to know more about the effect of disease states on systemic transit time dispersion.

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