scholarly journals Changes in regional myocardial volume during the cardiac cycle: implications for transmural blood flow and cardiac structure

2008 ◽  
Vol 295 (2) ◽  
pp. H610-H618 ◽  
Author(s):  
Hiroshi Ashikaga ◽  
Benjamin A. Coppola ◽  
Katrina G. Yamazaki ◽  
Francisco J. Villarreal ◽  
Jeffrey H. Omens ◽  
...  
Keyword(s):  
Blood Flow ◽  
Volume Change ◽  
Time Course ◽  
Cardiac Cycle ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Canine Heart ◽  
Spatiotemporal Resolution ◽  
Tissue Pressure

Although previous studies report a reduction in myocardial volume during systole, myocardial volume changes during the cardiac cycle have not been quantitatively analyzed with high spatiotemporal resolution. We studied the time course of myocardial volume in the anterior mid-left ventricular (LV) wall of normal canine heart in vivo ( n = 14) during atrial or LV pacing using transmurally implanted markers and biplane cineradiography (8 ms/frame). During atrial pacing, there was a significant transmural gradient in maximum volume decrease (4.1, 6.8, and 10.3% at subepi, midwall, and subendo layer, respectively, P = 0.002). The rate of myocardial volume increase during diastole was 4.7 ± 5.8, 6.8 ± 6.1, and 10.8 ± 7.7 ml·min−1·g−1, respectively, which is substantially larger than the average myocardial blood flow in the literature measured by the microsphere method (0.7–1.3 ml·min−1·g−1). In the early activated region during LV pacing, myocardial volume began to decrease before the LV pressure upstroke. We conclude that the volume change is greater than would be estimated from the known average transmural blood flow. This implies the existence of blood-filled spaces within the myocardium, which could communicate with the ventricular lumen. Our data in the early activated region also suggest that myocardial volume change is caused not by the intramyocardial tissue pressure but by direct impingement of the contracting myocytes on the microvasculature.

scholarly journals Asynchrony of ventricular activation affects magnitude and timing of fiber stretch in late-activated regions of the canine heart

2007 ◽  
Vol 293 (1) ◽  
pp. H754-H761 ◽  
Author(s):  
Benjamin A. Coppola ◽  
James W. Covell ◽  
Andrew D. McCulloch ◽  
Jeffrey H. Omens
Keyword(s):  
Aortic Valve ◽  
Time Course ◽  
Three Dimensional ◽  
Posterior Wall ◽  
Mechanical Dyssynchrony ◽  
Left Ventricular ◽  
Electrical Activation ◽  
Atrial Pacing ◽  
Canine Heart ◽  
Valve Opening

Abnormal electrical activation of the left ventricle results in mechanical dyssynchrony, which is in part characterized by early stretch of late-activated myofibers. To describe the pattern of deformation during “prestretch” and gain insight into its causes and sequelae, we implanted midwall and transmural arrays of radiopaque markers into the left ventricular anterolateral wall of open-chest, isoflurane-anesthetized, adult mongrel dogs. Biplane cineradiography (125 Hz) was used to determine the time course of two- and three-dimensional strains while pacing from a remote, posterior wall site. Strain maps were generated as a function of time. Electrical activation was assessed with bipolar electrodes. Posterior wall pacing generated prestretch at the measurement site, which peaked 44 ms after local electrical activation. Overall magnitudes and transmural gradients of strain were reduced when compared with passive inflation. Fiber stretch was larger at aortic valve opening compared with end diastole ( P < 0.05). Fiber stretch at aortic valve opening was weakly but significantly correlated with local activation time ( r2 = 0.319, P < 0.001). With a short atrioventricular delay, fiber lengths were not significantly different at the time of aortic valve opening during ventricular pacing compared with atrial pacing. However, ejection strain did significantly increase ( P < 0.05). We conclude that the majority of fiber stretch occurs after local electrical activation and mitral valve closure and is different from passive inflation. The increased shortening of these regions appears to be because of a reduced afterload rather than an effect of length-dependent activation in this preparation.

Transmural gradient of adenosine in canine heart during functional hyperemia

1991 ◽  
Vol 260 (3) ◽  
pp. H671-H680 ◽  
Author(s):  
A. Deussen ◽  
C. Walter ◽  
M. Borst ◽  
J. Schrader
Keyword(s):  
Oxygen Consumption ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Atrial Pacing ◽  
Canine Heart ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Transmural Gradient

Effects of beta-adrenergic stimulation and atrial pacing on the transmural gradient of intracellular free adenosine were assessed in dog hearts in vivo by measurement of the accumulation of S-adenosylhomocysteine (SAH) in the presence of homocysteine (1.6 mg.kg-1.min-1 iv). Isoproterenol (0.3-0.5 micrograms.kg-1.min-1 iv for 30 min) consistently enhanced left ventricular dP/dtmax (86%), heart rate (38%), and myocardial oxygen consumption (MVO2; 62%) within 3 min while formation and release of adenosine transiently increased. Diastolic aortic pressure fell from 107 +/- 12 to 58 +/- 5 mmHg, and the transmural gradient of SAH was 1.6-, 2.5-, and 4.4-fold increased in subepi-, mid- myo-, and subendocardial layers, respectively. Adenosine formation was inversely related to diastolic aortic pressure. Maintaining aortic pressure greater than 65 mmHg only slightly enhanced venoarterial difference of adenosine despite a greater augmentation of MVO2. Pacing the heart at 209 +/- 4 beats/min enhanced MVO2 by 42% and increased subepi-, midmyo-, and subendocardial levels of SAH by 1.5-, 3.3- and 1.9-fold, respectively. These results demonstrate that in the in situ heart 1) beta-adrenergic stimulation and pacing cause an inhomogeneous transmural increase in free intracellular adenosine mainly affecting the subendocardial and midmyocardial layers; 2) diastolic aortic pressure as the driving force of coronary perfusion is of critical importance for cardiac adenosine formation; and 3) the kinetics of oxygen consumption and adenosine formation are clearly dissociated during beta-stimulation.

scholarly journals High-speed volumetric two-photon fluorescence imaging of neurovascular dynamics

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Jiang Lan Fan ◽  
Jose A. Rivera ◽  
Wei Sun ◽  
John Peterson ◽  
Henry Haeberle ◽  
...  
Keyword(s):  
Blood Flow ◽  
High Speed ◽  
Laser Scanning ◽  
Three Dimensional ◽  
Laser Scanning Microscopy ◽  
Fluorescence Signal ◽  
Imaging Method ◽  
Spatiotemporal Resolution ◽  
Two Photon

AbstractUnderstanding the structure and function of vasculature in the brain requires us to monitor distributed hemodynamics at high spatial and temporal resolution in three-dimensional (3D) volumes in vivo. Currently, a volumetric vasculature imaging method with sub-capillary spatial resolution and blood flow-resolving speed is lacking. Here, using two-photon laser scanning microscopy (TPLSM) with an axially extended Bessel focus, we capture volumetric hemodynamics in the awake mouse brain at a spatiotemporal resolution sufficient for measuring capillary size and blood flow. With Bessel TPLSM, the fluorescence signal of a vessel becomes proportional to its size, which enables convenient intensity-based analysis of vessel dilation and constriction dynamics in large volumes. We observe entrainment of vasodilation and vasoconstriction with pupil diameter and measure 3D blood flow at 99 volumes/second. Demonstrating high-throughput monitoring of hemodynamics in the awake brain, we expect Bessel TPLSM to make broad impacts on neurovasculature research.

Impact of ejection on magnitude and time course of ventricular pressure-generating capacity

1993 ◽  
Vol 265 (3) ◽  
pp. H899-H909 ◽  
Author(s):  
D. Burkhoff ◽  
P. P. De Tombe ◽  
W. C. Hunter
Keyword(s):  
Time Course ◽  
Cardiac Cycle ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Time Varying ◽  
Generating Capacity ◽  
Ejection Phase ◽  
Time Point ◽  
Ventricular Dynamics

This study focuses on elucidating how ventricular afterloading conditions affect the time course of change of left ventricular pressure (LVP) throughout the cardiac cycle, with particular emphasis on revealing specific limitations in the time-varying elastance model of ventricular dynamics. Studies were performed in eight isolated canine hearts ejecting into a simulated windkessel afterload. LVP waves measured (LVPm) during ejection were compared with those predicted (LVPpred) according to the elastance theory. LVPm exceeded LVPpred from a time point shortly after the onset of ejection to the end of the beat. The instantaneous difference between LVPm and LVPpred increased steadily as ejection proceeded and reached between 45 and 65 mmHg near end ejection. This was in large part due to an average 35-ms prolongation of the time to end systole (tes) in ejecting compared with isovolumic beats. The time constant of relaxation was decreased on ejecting beats so that, despite the marked prolongation of tes, the overall duration of ejecting contractions was not greater than that of isovolumic beats. The results demonstrate a marked ejection-mediated enhancement and prolongation of ventricular pressure-generating capacity during the ejection phase of the cardiac cycle with concomitant acceleration of relaxation. None of these factors are accounted for by the time-varying elastance theory.

Myocardial volume change during cardiac cycle derived from three orthogonal systolic strains: towards a quality assessment of strains

2018 ◽  
Vol 60 (3) ◽  
pp. 286-292 ◽  
Author(s):  
Laurent Bonnemains ◽  
Anne Sophie Guerard ◽  
Paul Soulié ◽  
Freddy Odille ◽  
Jacques Felblinger
Keyword(s):  
Left Ventricle ◽  
Quality Assessment ◽  
Healthy Volunteers ◽  
Volume Change ◽  
Cardiac Cycle ◽  
Mean Value ◽  
Left Ventricular ◽  
Strain Measurements ◽  
Significant Difference ◽  
Standard Deviations

Background The relative modification of the myocardial volume between end-systole and end-diastole ([Formula: see text]) has already been assessed with different methods and falls in a range of 0.9–0.97 (mean value = 0.93). Purpose To estimate [Formula: see text] from the three longitudinal ([Formula: see text], circumferential ([Formula: see text]), and radial ([Formula: see text]) strains of the left ventricle using the formula: [Formula: see text] and to test whether this estimate of [Formula: see text] can be used as a marker of the echocardiography quality. Material and Methods Two hundred manuscripts, including a total of 34,690 patients or healthy volunteers, were identified in the Medline database containing values of [Formula: see text], [Formula: see text], and [Formula: see text] measured from echocardiography. Results The median value of was 0.93, in accordance with the literature, with no significant difference between patients or healthy volunteers ( P = 0.38). The proportion of studies with [Formula: see text] was 79%. When only considering groups of healthy volunteers, the studies failing this test had higher standard deviations for the three individual strains: 0.038 vs. 0.029 ( P = 0.02) for [Formula: see text]; 0.060 vs. 0.034 ( P < 10–6) for [Formula: see text], and 0.243 vs. 0.101 ( P < 10–14) for [Formula: see text]. Conclusion The median ratio of the left ventricular myocardial volumes between end-systole and end-diastole in the investigated studies was [Formula: see text]. The formula [Formula: see text] could be used to detect studies with inaccurate strain measurements.

Numerical study of hemodynamics after stent implantation during the cardiac cycle

2021 ◽  
Vol 15 (2) ◽  
pp. 8016-8028
Author(s):  
Abdelhakem Belaghit ◽  
B. Aour ◽  
M. Larabi ◽  
A. A. Tadjeddine ◽  
S. Mebarki
Keyword(s):  
Blood Flow ◽  
Stent Implantation ◽  
Cardiac Cycle ◽  
Numerical Study ◽  
Shear Stresses ◽  
Flow Profile ◽  
Hemodynamic State ◽  
Dynamics Simulations ◽  
Medical Planning

The descending aortic aneurysm is one of the most catastrophic cardiovascular emergencies resulting in high mortality worldwide. Clinical observations have pointed out that stent implantation in the sick aorta should probably allow stabilization of the hemodynamic state of the patient's aorta. To better understand the hemodynamic impact of a stent-treated aneurysm, numerical simulations are used to evaluate hemodynamic parameters. These latter including flow profile, velocity distribution, aortic wall pressure and shear stress, which are difficult to measure in vivo. It should be noted that the numerical modeling assists in medical planning by providing patterns of blood circulation, in particular, the distribution of pressures and shear stresses in the wall. In this context, the pulsatile blood flow in the aneurysmal aorta with stent is studied by CFD (Computational Fluid Dynamics) simulations. Realistic boundary conditions time dependent are prescribed at the level of the different arteries of the complete aorta models. The hemodynamic profile of the aneurysmal aorta with stent was analyzed by contour planes of velocity vectors, pressures and shear stresses at different times during the cardiac cycle. The obtained results made it possible to show the effect of the stent on the improvement of the blood flow by solving the problems of hemodynamic disturbances in the aorta.  The methodology used in this work has revealed detailed and necessary information for the cases studied and shows the interest of the numerical tool for diagnosis and surgery.

Steady-state catecholamine stimulation does not increase cytosolic adenosine in canine hearts

1994 ◽  
Vol 266 (2) ◽  
pp. H503-H510
Author(s):  
K. Kroll ◽  
G. V. Martin
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Myocardial Blood Flow ◽  
Left Ventricular ◽  
Control Group ◽  
Atrial Pacing ◽  
Homocysteine Thiolactone ◽  
Rate Dependent ◽  
Unstimulated Control ◽  
Metabolic Stimulation

Myocardial adenosine production increases transiently during the onset of catecholamine stimulation; however, there is conflicting evidence regarding whether cytosolic adenosine concentrations are increased during sustained steady-state stimulation. If cytosolic adenosine is not elevated during steady-state stimulation, then adenosine produced in the cytosol does not play a role in mediating the sustained increase in myocardial blood flow. The purpose of the present study was to determine whether cytosolic adenosine concentrations in the anesthetized dog heart are increased during steady-state stimulation with norepinephrine, epinephrine, and atrial pacing. Regional cytosolic adenosine concentrations were assessed by measuring myocardial content of S-adenosyl-L-homocysteine (SAH) after 20 min of intravenous administration of L-homocysteine thiolactone. Excess homocysteine causes myocardial accumulation of SAH at a rate dependent on the cytosolic concentration of adenosine. Steady-state metabolic stimulation caused more than twofold increases in myocardial blood flow and oxygen consumption, but there was no increase in left ventricular content of SAH in the stimulation group [6.3 +/- 0.9 nmol/g (SE); n = 6] relative to a parallel unstimulated control group (6.4 +/- 0.9 nmol/g; n = 6). The transmural distribution of SAH was nearly uniform, and there was no correlation between regional measurements of blood flow and myocardial content of SAH or ATP either during metabolic stimulation or under control conditions. In separate experiments, myocardial ischemia caused fivefold increases in SAH content, confirming the sensitivity of the SAH method for increased cytosolic adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)

Tachycardia-induced cardiomyopathy: effects on blood flow and capillary structure

1991 ◽  
Vol 261 (1) ◽  
pp. H140-H148 ◽  
Author(s):  
F. G. Spinale ◽  
J. L. Zellner ◽  
M. Tomita ◽  
G. E. Tempel ◽  
F. A. Crawford ◽  
...  
Keyword(s):  
Blood Flow ◽  
Capillary Density ◽  
Left Ventricular ◽  
Lv Function ◽  
Atrial Pacing ◽  
Capillary Structure ◽  
Potential Factor ◽  
Rapid Pacing ◽  
Tachycardia Induced Cardiomyopathy ◽  
Fractional Shortening

Chronic supraventricular tachycardia (SVT) causes a dilated cardiomyopathy. A potential factor contributing to the development of SVT-induced cardiomyopathy is abnormal myocardial blood flow (MBF). The purpose of this study was to relate changes in left ventricular (LV) function, MBF, and capillary structure with the development of SVT-induced cardiomyopathy. LV function and MBF were measured in two groups of conscious pigs: sham control (CON; n = 8) and after 3 wk of atrial pacing (SVT; 240 beats/min; n = 8) using echocardiography-catheterization and microspheres. Measurements were made under three states: 1) at rest with a basal heart rate, 2) during rapid atrial pacing (240 beats/min), and 3) during adenosine infusion (1.5 microM.kg-1.min-1) without pacing. LV capillary density, diameter, wall thickness, and capillary-myocyte distance were measured in four additional pigs from each group. LV fractional shortening was lower, and left atrial pressure was significantly higher in the SVT group compared with CON at rest, during pacing, and with adenosine (P less than 0.05). In the CON group, average LV-MBF at rest was 2.0 +/- 0.2 ml.min-1.g-1, increased with pacing to 3.0 +/- 0.2 ml.min-1.g-1 (P less than 0.05), and increased further with adenosine to 4.1 +/- 0.3 ml.min-1.g-1 (P less than 0.05). In all states, SVT LV-MBF was significantly reduced vs. CON (P less than 0.05); SVT LV-MBF was 0.8 +/- 0.2 ml.min-1.g-1 at rest, increased to 1.3 +/- 0.3 ml.min-1.g-1 with rapid pacing (P less than 0.05), and remained unchanged during adenosine (1.3 +/- 0.4 ml.min-1.g-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary smooth muscle reactivity to muscarinic stimulation after ischemia-reperfusion in porcine myocardial infarction

2003 ◽  
Vol 95 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Antonio Rodríguez-Sinovas ◽  
Josep Bis ◽  
Inocencio Anivarro ◽  
Javier de la Torre ◽  
Antoni Bayés-Genís ◽  
...  
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Severe Left Ventricular Dysfunction ◽  
Coronary Smooth Muscle

This study tested whether ischemia-reperfusion alters coronary smooth muscle reactivity to vasoconstrictor stimuli such as those elicited by an adventitial stimulation with methacholine. In vitro studies were performed to assess the reactivity of endothelium-denuded infarct-related coronary arteries to methacholine ( n = 18). In addition, the vasoconstrictor effects of adventitial application of methacholine to left anterior descending (LAD) coronary artery was assessed in vivo in pigs submitted to 2 h of LAD occlusion followed by reperfusion ( n = 12), LAD deendothelization ( n = 11), or a sham operation ( n = 6). Endothelial-dependent vasodilator capacity of infarct-related LAD was assessed by intracoronary injection of bradykinin ( n = 13). In vitro, smooth muscle reactivity to methacholine was unaffected by ischemia-reperfusion. In vivo, baseline methacholine administration induced a transient and reversible drop in coronary blood flow (9.6 ± 4.6 to 1.9 ± 2.6 ml/min, P < 0.01), accompanied by severe left ventricular dysfunction. After ischemia-reperfusion, methacholine induced a prolonged and severe coronary blood flow drop (9.7 ± 7.0 to 3.4 ± 3.9 ml/min), with a significant delay in recovery ( P < 0.001). Endothelial denudation mimics in part the effects of methacholine after ischemia-reperfusion, and intracoronary bradykinin confirmed the existence of endothelial dysfunction. Infarct-related epicardial coronary artery shows a delayed recovery after vasoconstrictor stimuli, because of appropriate smooth muscle reactivity and impairment of endothelial-dependent vasodilator capacity.

Sign in / Sign up

Export Citation Format

Share Document