scholarly journals Overview of mathematical modeling of myocardial blood flow regulation

2020 ◽  
Vol 318 (4) ◽  
pp. H966-H975
Author(s):  
Ravi Namani ◽  
Yoram Lanir ◽  
Lik Chuan Lee ◽  
Ghassan S. Kassab
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Oxygen Demand ◽  
Flow Regulation ◽  
Flow Reserve ◽  
Arterial Blood ◽  
Blood Flow Regulation ◽  
Highly Nonlinear ◽  
Coronary Flow Regulation

The oxygen consumption by the heart and its extraction from the coronary arterial blood are the highest among all organs. Any increase in oxygen demand due to a change in heart metabolic activity requires an increase in coronary blood flow. This functional requirement of adjustment of coronary blood flow is mediated by coronary flow regulation to meet the oxygen demand without any discomfort, even under strenuous exercise conditions. The goal of this article is to provide an overview of the theoretical and computational models of coronary flow regulation and to reveal insights into the functioning of a complex physiological system that affects the perfusion requirements of the myocardium. Models for three major control mechanisms of myogenic, flow, and metabolic control are presented. These explain how the flow regulation mechanisms operating over multiple spatial scales from the precapillaries to the large coronary arteries yield the myocardial perfusion characteristics of flow reserve, autoregulation, flow dispersion, and self-similarity. The review not only introduces concepts of coronary blood flow regulation but also presents state-of-the-art advances and their potential to impact the assessment of coronary microvascular dysfunction (CMD), cardiac-coronary coupling in metabolic diseases, and therapies for angina and heart failure. Experimentalists and modelers not trained in these models will have exposure through this review such that the nonintuitive and highly nonlinear behavior of coronary physiology can be understood from a different perspective. This survey highlights knowledge gaps, key challenges, future research directions, and novel paradigms in the modeling of coronary flow regulation.

scholarly journals Early Hyperdynamic Sepsis Alters Coronary Blood Flow Regulation in Porcine Fecal Peritonitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Céline Boudart ◽  
Fuhong Su ◽  
Lorenzo Pitisci ◽  
Arnaud Dhoine ◽  
Olivier Duranteau ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Ex Vivo ◽  
Flow Regulation ◽  
Flow Reserve ◽  
Vasodilatory Response ◽  
Blood Flow Regulation ◽  
Microvascular Resistance ◽  
Hyperdynamic Sepsis

Background: Sepsis is a common condition known to impair blood flow regulation and microcirculation, which can ultimately lead to organ dysfunction but such contribution of the coronary circulation remains to be clarified. We investigated coronary blood flow regulatory mechanisms, including autoregulation, metabolic regulation, and endothelial vasodilatory response, in an experimental porcine model of early hyperdynamic sepsis.Methods: Fourteen pigs were randomized to sham (n = 7) or fecal peritonitis-induced sepsis (n = 7) procedures. At baseline, 6 and 12 h after peritonitis induction, the animals underwent general and coronary hemodynamic evaluation, including determination of autoregulatory breakpoint pressure and adenosine-induced maximal coronary vasodilation for coronary flow reserve and hyperemic microvascular resistance calculation. Endothelial-derived vasodilatory response was assessed both in vivo and ex vivo using bradykinin. Coronary arteries were sampled for pathobiological evaluation.Results: Sepsis resulted in a right shift of the autoregulatory breakpoint pressure, decreased coronary blood flow reserve and increased hyperemic microvascular resistance from the 6th h after peritonitis induction. In vivo and ex vivo endothelial vasomotor function was preserved. Sepsis increased coronary arteries expressions of nitric oxide synthases, prostaglandin I2 receptor, and prostaglandin F2α receptor.Conclusion: Autoregulation and metabolic blood flow regulation were both impaired in the coronary circulation during experimental hyperdynamic sepsis, although endothelial vasodilatory response was preserved.

Myocardial blood flow and coronary reserve in chronically anemic fetal lambs

1999 ◽  
Vol 277 (1) ◽  
pp. R306-R313 ◽  
Author(s):  
Lowell E. Davis ◽  
A. Roger Hohimer ◽  
Mark J. Morton
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Adenosine Infusion ◽  
Fetal Sheep ◽  
Coronary Reserve ◽  
Flow Reserve ◽  
Coronary Conductance ◽  
The Difference

Chronic fetal anemia produces large compensatory increases in coronary blood flow in the near-term fetal lamb. To determine if increased coronary flow in anemic fetuses is associated with decreased coronary flow reserve or, alternatively, an increase in coronary conductance, we measured maximal coronary artery conductance during adenosine infusion before and during anemia. Isovolemic hemorrhage over 7 days reduced hematocrit from 30.6 ± 2.7 to 15.8 ± 2.4% ( P < 0.02) and the oxygen content from 7.3 ± 1.4 to 2.6 ± 0.4 ml/dl ( P < 0.001). Coronary blood flow increased from control (202 ± 60) to 664 ± 208 ml ⋅ min−1 ⋅ 100 g−1 with adenosine to 726 ± 169 ml ⋅ min−1 ⋅ 100 g−1 during anemia and to 1,162 ± 250 ml ⋅ min−1 ⋅ 100 g−1 (left ventricle) during anemia with adenosine infusion (all P< 0.001). Coronary conductance, determined during maximal vasodilation, was 18.2 ± 7.7 before and 32.8 ± 11.9 ml ⋅ min−1 ⋅ 100 g−1 ⋅ mmHg−1during anemia ( P < 0.001). Coronary reserve, the difference between resting and maximal myocardial blood flow interpolated at 40 mmHg, was unchanged in control and anemic fetuses (368 ± 142 and 372 ± 201 ml/min). Because hematocrit affects viscosity, anemic fetuses were transfused with blood to acutely increase the hematocrit back to control, and conductance was remeasured. Coronary blood flow decreased 57.3 ± 18.9% but was still 42.6 ± 18.9% greater than control. We conclude that in chronically anemic fetal sheep coronary conductance is increased and coronary reserve is maintained, and this is attributed in part to angiogenesis as well as changes in viscosity.

Preliminary observations on blood flow in the coronary arteries of two school sharks (Galeorhinus australis)

1993 ◽  
Vol 71 (6) ◽  
pp. 1238-1241 ◽  
Author(s):  
Peter S. Davie ◽  
Craig E. Franklin
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Cardiac Cycle ◽  
Arterial Blood Flow ◽  
Ventricular Systole ◽  
Arterial Blood ◽  
Ventricular Mass ◽  
Aortic Blood Velocity

Coronary arterial blood flow and pressure, intraventricular blood pressure, and ventral aortic blood velocity were measured in two anaesthetized school sharks (Galeorhinus australis) in order to examine the phasic relationships between these flows and pressures. Maximum instantaneous flow recorded in the ventral coronary artery was 0.37 mL∙min−1∙kg−1 body mass (estimated 0.63 mL∙min−1∙g−1 ventricular mass). The average mean coronary blood flow was estimated as 0.28 mL∙min−1∙g−1 ventricular mass during periods of high coronary blood flow. On average, 86% of coronary flow occurred during diastole. Coronary arterial flow began during the last quarter of ventricular systole. Coronary blood flow peaked when intraventricular pressure fell to just below zero immediately after ventricular systole. Coronary blood flow fell slightly as diastole continued and reflected the small fall in coronary arterial pressure. Coronary flow reversed briefly during isovolumic ventricular contraction. Increases in the proportion of the cardiac cycle occupied by ventricular diastole, which occur during hypoxic bradycardia, have the potential to more than double coronary blood flow provided coronary arterial pressure is maintained.

Coronary blood flow regulation in exercising swine involves parallel rather than redundant vasodilator pathways

2003 ◽  
Vol 285 (1) ◽  
pp. H424-H433 ◽  
Author(s):  
Daphne Merkus ◽  
David B. Haitsma ◽  
Tse-Yeung Fung ◽  
Yvette J. Assen ◽  
Pieter D. Verdouw ◽  
...  
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Adenosine Receptors ◽  
Flow Regulation ◽  
The Other ◽  
Vasodilator Reserve ◽  
Redundancy Design ◽  
Oxide Synthase ◽  
Coronary Flow Regulation ◽  
Metabolic Vasodilation

In dogs, only combined blockade of vasodilator pathways [via adenosine receptors, nitric oxide synthase (NOS) and ATP-sensitive K+ (KATP) channels] results in impairment of metabolic vasodilation, which suggests a redundancy design of coronary flow regulation. Conversely, in swine and humans, blocking KATP channels, adenosine receptors, or NOS each impairs coronary blood flow (CBF) at rest and during exercise. Consequently, we hypothesized that these vasodilators act in parallel rather than in redundancy to regulate CBF in swine. Swine exercised on a treadmill (0–5 km/h), during control and after blockade of KATP channels (with glibenclamide), adenosine receptors [with 8-phenyltheophylline (8-PT)], and/or NOS [with Nω-nitro-l-arginine (l-NNA)]. l-NNA, 8-PT, and glibenclamide each reduced myocardial O2 delivery and coronary venous O2 tension. These effects of l-NNA, 8-PT, and glibenclamide were not modified by simultaneous blockade of the other vasodilators. Combined blockade of KATP channels and adenosine receptors with or without NOS inhibition was associated with increased H+ production and impaired myocardial function. However, despite an increase in O2 extraction to >90% during administration of l-NNA + 8-PT + glibenclamide, vasodilator reserve could still be recruited during exercise. Thus in awake swine, loss of KATP channels, adenosine, or NO is not compensated for by increased participation of the other two vasodilator mechanisms. These findings suggest a parallel rather than a redundancy design of CBF regulation in the porcine circulation.

Regulation of coronary flow

2021 ◽  
pp. 11-13
Author(s):  
Nico Bruining ◽  
Eric Boersma ◽  
Dirk J. Duncker
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Arterial Blood ◽  
Arterial Inflow ◽  
Systolic Phase ◽  
Vascular Beds

This chapter describes the regulation of coronary blood flow. The left ventricle generates the systemic arterial blood pressure that is required to maintain coronary blood flow. The coronary circulation is unique among regional vascular beds in that its perfusion is impeded during the systolic phase of the cardiac cycle by the surrounding contracting cardiac muscle. Systolic contraction increases left ventricular wall tension and compresses the intramyocardial microvessels, thereby impeding coronary arterial inflow. This compression is not uniformly distributed across the left ventricular wall, resulting in a redistribution of blood flow from the subendocardium to subepicardium.

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