Myoglobin function in the isolated fluorocarbon-perfused dog heart

1978 ◽  
Vol 234 (5) ◽  
pp. H567-H572 ◽  
Author(s):  
R. P. Cole ◽  
B. A. Wittenberg ◽  
P. R. Caldwell
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricle ◽  
Mechanical Performance ◽  
Left Ventricular Pressure ◽  
Dry Weight ◽  
Left Ventricular ◽  
Facilitated Diffusion ◽  
Dog Heart ◽  
Before And After ◽  
Ringer’S Lactate

An isolated dog heart preparation perfused with hemoglobin-free fluorocarbon suspension has been developed to study the role of myoglobin in myocardial function. The coronary vasculature was perfused at constant flow, with oxygen consumption determined from arteriovenous PO2 differences. Muscle function was assessed by measurement of pressures generated in a latex balloon placed in the left ventricle. The perfusate consisted of 20% perfluorotributylamine and 80% Ringer's lactate with 16 mM glucose. Steady-state oxygen consumption decreased from 0.30 to 0.11 ml/min per gram dry weight left ventricle, as perfusate PO2 decreased from 690 to 150 mmHg. Left ventricular pressure generation and oxygen consumption were determined before and after addition of 8 mM sodium nitrite, which changed functional ferrous myoglobin to high-spin ferric myoglobin. Over the range of perfusate PO2 studied, nitrite addition did not alter mechanical performance or myocardial oxygen consumption. These data suggest that those conditions necessary for substantial myoglobin-facilitated diffusion of oxygen in the myocardium are not present in the isolated fluorocarbon-perfused dog heart.

Heart rate-independent energetics and systolic pressure-volume area in dog heart

1983 ◽  
Vol 244 (2) ◽  
pp. H206-H214 ◽  
Author(s):  
H. Suga ◽  
R. Hisano ◽  
S. Hirata ◽  
T. Hayashi ◽  
O. Yamada ◽  
...  
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Left Ventricle ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Canine Heart ◽  
Heart Rates ◽  
Dog Heart ◽  
Total Mechanical Energy

Left ventricular (LV) systolic pressure-volume area (PVA), a new measure of total mechanical energy for the contraction, linearly correlates with its oxygen consumption per beat (VO2) regardless of contraction mode in a canine heart with stable chronotropism and inotropism. PVA is the area in the pressure-volume (PV) diagram circumscribed by the end-systolic and end-diastolic PV relation curves and the systolic segment of the PV loop and has dimensions of energy. We investigated whether primary changes in heart rate would affect the VO2-PVA relation. In the excised cross-circulated canine heart with left ventricular load controlled with a servo pump, we changed heart rate by pacing to compare the VO2-PVA relations at low [124 +/- 17 (SD) min-1] and high (193 +/- 23) heart rates. In 15 left ventricles, VO2 (ml O2 X beat-1 X 100 g LV-1) was (1.75 +/- 0.57) X 10(-5) PVA (mmHg X ml X beat-1 X 100 g LV-1) + 0.031 +/- 0.011 (ml O2 X beat-1 X 100 g LV-1). The VO2-PVA relation was virtually independent of heart rate in individual hearts. We conclude that the load-independent VO2-PVA relationship is not affected by chronotropism in a given canine left ventricle.

Effects of anodal vs. cathodal pacing on the mechanical performance of the isolated rabbit heart

2000 ◽  
Vol 89 (3) ◽  
pp. 1159-1164 ◽  
Author(s):  
Anshul Thakral ◽  
Louis H. Stein ◽  
Mahesh Shenai ◽  
Boris I. Gramatikov ◽  
Nitish V. Thakor
Keyword(s):  
Left Ventricle ◽  
Mechanical Response ◽  
Mechanical Performance ◽  
Balloon Catheter ◽  
Left Ventricular Pressure ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Maximum Pressure ◽  
Anodal Stimulation

Previous studies have suggested that anodal pacing enhances electrical conduction in the heart near the pacing site. It was hypothesized that enhanced conduction by anodal pacing would also enhance ventricular pressure in the heart. Left ventricular pressure measurements were made in isolated, Langendorff-perfused rabbit hearts by means of a Millar pressure transducer with the use of a balloon catheter fixed in the left ventricle. The pressure wave was analyzed for maximum pressure (Pmax) generated in the left ventricle and the work done by the left ventricle (Parea). Eight hearts were paced with monophasic square-wave pulses of varying amplitudes (2, 4, 6, and 8 V) with 100 pulses of each waveform delivered to the epicardium. Anodal stimulation pulses showed statistically significant improvement in mechanical response at 2, 4, and 8 V. Relative to unipolar cathodal pacing, unipolar anodal pacing improved Pmax by 4.4 ± 2.3 (SD), 5.3 ± 3.1, 3.5 ± 4.9, and 4.8 ± 1.9% at 2, 4, 6, and 8 V, respectively. Unipolar anodal stimulation also improved Parea by 9.0 ± 3.0, 12.0 ± 6.0, 10.1 ± 7.7, and 11.9 ± 6.0% at 2, 4, 6, and 8 V, respectively. Improvements in Pmax and Parea indicate that an anodally paced heart has a stronger mechanical response than does a cathodally paced heart. Anodal pacing might be useful as a novel therapeutic technology to treat mechanically impaired or failed hearts.

Clinical and Experimental Analysis of 201Thallium Uptake of the Heart

1978 ◽  
Vol 17 (04) ◽  
pp. 142-148
Author(s):  
U. Büll ◽  
S. Bürger ◽  
B. E. Strauer
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricle ◽  
Muscle Mass ◽  
Myocardial Oxygen Consumption ◽  
Animal Experiments ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Flow Measurements ◽  
Myocardial Flow

Studies were carried out in order to determine the factors influencing myocardial 201T1 uptake. A total of 158 patients was examined with regard to both 201T1 uptake and the assessment of left ventricular and coronary function (e. g. quantitative ventriculography, coronary arteriography, coronary blood flow measurements). Moreover, 42 animal experiments (closed chest cat) were performed. The results demonstrate that:1) 201T1 uptake in the normal and hypertrophied human heart is linearly correlated with the muscle mass of the left ventricle (LVMM);2) 201T1 uptake is enhanced in the inner (subendocardial) layer and is decreased in the outer (subepicardial) layer of the left ventricular wall. The 201T1 uptake of the right ventricle is 40% lower in comparison to the left ventricle;3) the basic correlation between 201T1 uptake and LVMM is influenced by alterations of both myocardial flow and myocardial oxygen consumption; and4) inotropic interventions (isoproterenol, calcium, norepinephrine) as well as coronary dilatation (dipyridamole) may considerably augment 201T1 uptake in accordance with changes in myocardial oxygen consumption and/or myocardial flow.It is concluded that myocardial 201T1 uptake is determined by multiple factors. The major determinants have been shown to include (i) muscle mass, (ii) myocardial flow and (iii) myocardial oxygen consumption. The clinical data obtained from patient groups with normal ventricular function, with coronary artery disease, with left ventricular wall motion abnormalities and with different degree of left ventricular hypertrophy are correlated with quantitated myocardial 201T1 uptake.

Positive inotropism in hypothermia partially depends on an increase in maximal Ca(2+)-activated force

1991 ◽  
Vol 261 (4) ◽  
pp. H1005-H1010 ◽  
Author(s):  
H. Kusuoka ◽  
Y. Ikoma ◽  
S. Futaki ◽  
H. Suga ◽  
A. Kitabatake ◽  
...  
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Oxygen Consumption ◽  
Mild Hypothermia ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Phosphorus Compounds ◽  
Resonance Spectroscopy ◽  
Positive Inotropism ◽  
Rapid Pacing ◽  
Intact Heart

We investigated the contribution of maximal Ca(2+)-activated force to the positive inotropism induced by mild hypothermia. Phosphorus-31 nuclear magnetic resonance spectroscopy revealed that neither energy-related phosphorus compounds in myocardium nor intracellular pH was responsible for the change in contractility. Maximal Ca(2+)-activated pressure (MCAP), the intact-heart correlate of maximal Ca(2+)-activated force, was determined in isolated perfused rabbit hearts by measuring isovolumic left ventricular pressure during tetani at extracellular Ca2+ concentrations greater than or equal to 10 mM. Tetani were elicited by rapid pacing after exposure to ryanodine. MCAP increased by 2.17 +/- 0.28% (mean +/- SE, P less than 0.001, n = 19) for each degree of myocardial cooling between 30 and 38 degrees C. Our results indicate that a primary change in myofilament Ca2+ responsiveness underlies the positive inotropism in hypothermia. The increase in maximal Ca(2+)-activated force may explain the observation of positive inotropism without an upward shift in the relation between oxygen consumption and pressure-volume area, as previously reported for cooled whole hearts.

Severe diastolic dysfunction with preserved energy conversion efficiency after countershock

1997 ◽  
Vol 273 (2) ◽  
pp. H583-H592 ◽  
Author(s):  
S. Yasuda ◽  
T. Shishido ◽  
Y. Goto
Keyword(s):  
Diastolic Dysfunction ◽  
Mechanical Performance ◽  
Diastolic Pressure ◽  
Mechanical Energy ◽  
Systolic Pressure ◽  
Myocardial Edema ◽  
Energy Conversion Efficiency ◽  
Left Ventricular ◽  
Stunned Myocardium ◽  
Before And After

The left ventricular (LV) mechanical performance and the LV myocardial oxygen consumption (VO2)-to-pressure-volume area (PVA; LV total mechanical energy index) relationship were measured in isovolumic contraction of isolated blood-perfused dog hearts before and after direct current (DC) countershocks. At a constant LV volume, DC shocks increased LV end-diastolic pressure progressively and strikingly with the progression of myocardial edema and a marked prolongation of the time constant of LV pressure decay. In contrast, DC shocks changed neither the slope of the LV end-systolic pressure-volume relationship nor the contractile efficiency (the slope of the Vo2-PVA relationship). The oxygen cost of contractility (the slope of the relationship between PVA-independent VO2 and LV contractility) increased 27% after DC shocks. However, the magnitude of this change was considerably smaller than that previously reported in postischemic stunned myocardium (123%), suggesting that the adverse effect of DC shocks on the energy cost of excitation-contraction coupling is relatively minor. Thus, despite the severe diastolic dysfunction, DC shocks do not substantially impair either the efficiency of cross-bridge cycling or calcium cycling. Myocardial interstitial edema is more likely a potential mechanism of diastolic dysfunction after DC shocks.

Fluid-Structure Interaction Simulation of Blood Flow Inside a Diseased Left Ventricle With Obstructive Hypertrophic Cardiomyopathy in Early Systole

2009 ◽  
Author(s):  
Ahmad Moghaddaszade-Kermani ◽  
Peter Oshkai ◽  
Afzal Suleman
Keyword(s):  
Blood Flow ◽  
Hypertrophic Cardiomyopathy ◽  
Left Ventricle ◽  
Fluid Structure Interaction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Fluid Structure ◽  
Structure Interaction ◽  
Systolic Phase

Mitral-Septal contact has been proven to be the cause of obstruction in the left ventricle with hypertrophic cardiomyopathy (HC). This paper presents a study on the fluid mechanics of obstruction using two-way loosely coupled fluid-structure interaction (FSI) methodology. A parametric model for the geometry of the diseased left ventricular cavity, myocardium and mitral valve has been developed, using the dimensions extracted from magnetic resonance images. The three-element Windkessel model [1] was modified for HC and solved to introduce pressure boundary condition to the aortic aperture in the systolic phase. The FSI algorithm starts at the beginning of systolic phase by applying the left ventricular pressure to the internal surface of the myocardium to contract the muscle. The displacements of the myocardium and mitral leaflets were calculated using the nonlinear finite element hyperelastic model [2] and subsequently transferred to the fluid domain. The fluid mesh was moved accordingly and the Navier-Stokes equations were solved in the laminar regime with the new mesh using the finite volume method. In the next time step, the left ventricular pressure was increased to contract the muscle further and the same procedure was repeated for the fluid solution. The results show that blood flow jet applies a drag force to the mitral leaflets which in turn causes the leaflet to deform toward the septum thus creating a narrow passage and possible obstruction.

scholarly journals NT-proBNP level and left ventricle diameters before and after transcatheter closure of PDA and VSD

2018 ◽  
Vol 58 (5) ◽  
pp. 213-20
Author(s):  
Devy Kusmira ◽  
Ria Nova ◽  
Achirul Bakri
Keyword(s):  
Left Ventricle ◽  
Transcatheter Closure ◽  
Ductus Arteriosus ◽  
Left Ventricular ◽  
Internal Diameter ◽  
Positive Correlation ◽  
Amino Terminal ◽  
Muscle Stretching ◽  
Before And After ◽  
Moderate Positive Correlation

Background Amino-terminal pro-B-type natriuretic peptide (NT-proBNP) levels before and after transcatheter closure may correlate with changes in left ventricular internal diameter end diastole (LVIDd) and end systole (LVIDs). Patent ductus arteriosus (PDA) and ventricular septal defect (VSD) are structural abnormalities which effects cardiac hypertrophy. Cardiac muscle stretching decreases after closure, followed by reduced left ventricle diameters and decreased NT-proBNP levels. Objective To analyze for possible correlations between NT-proBNP levels and left ventricle diameters before and after transcatheter closure. Methods Subjects were PDA and VSD patients who underwent transcatheter closure in the Pediatrics Department of dr. Moh Hoesin Hospital, Palembang, South Sumatera, from May 2016 to March 2017. Measurement of NT-proBNP levels and echocardiography were performed before closure, as well as one and three months after closure. Results There were 34 subjects (15 girls) with median age of 91.5 months. Median NT-proBNP levels were significantly reduced after closure: before closure 111.7pg/mL, one month after closure 62pg/mL, and three months after closure 39 pg/mL (P<0.05). Median LVIDd and LVIDs were also significantly reduced after closure [LVIDd: 39.5mm before, 34.5mm one mo after, and 32.5mm 3 mo after (P<0.05); LVIDs: 23.9mm before, 20.5mm 1 mo after, and 20.0mm 3 mo after (P<0.05)]. At one month after closure, there was a moderate positive correlation between NT-proBNP levels and LVIDd (r=0.432; P=0.011), but no correlation with LVIDs (r=0.287; P=0.100). At three months after closure, there was a significant moderate positive correlation between changes of NT-proBNP levels and changes of LVIDd (r=0.459; P=0.006), as well as LVIDs (r=0.563; P=0.001). Conclusion In pediatric PDA and VSD patients, NT-proBNP levels have a significant positive correlation with diastolic and systolic left ventricle diameters at three months after closure. Decreased NT-proBNP levels may be considered as a marker of closure effectiveness.

Left Intraventricular Balloon Pump Optimization during Intractable Cardiac Arrest

1996 ◽  
Vol 19 (7) ◽  
pp. 422-430 ◽  
Author(s):  
S.F. Stamatelopoulos ◽  
L. Kochilas ◽  
N.S. Saridakis ◽  
N.A. Zakopoulos ◽  
S.D. Moulopoulos
Keyword(s):  
Cardiac Arrest ◽  
Left Ventricle ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Hemodynamic Effect ◽  
Dog Heart ◽  
End Diastolic Volume

This work aims to determine optimal balloon shape and volume during left intraventricular balloon pumping (IABP) in the fibrillating dog heart. A balloon volume equal to the left ventricular end-diastolic volume (LVEDV) maintained a higher systolic aortic pressure and flow (106.4 ± 2.7 mmHg and 84.7 ± 2.35 ml/kg/min, x ± SEM, respectively) than a 25% smaller (97.8 ± 3.3 mmHg, P=0.002 and 63.7 ± 4.1 ml/Kg/min, P=0.002, respectively) or a 25% larger balloon (87.4 ± 2.3 mmHg, P=0.002 and 70.9 ± 3.4 ml/kg/min, P=0.002, respectively). Among 5 different balloon shapes tested, a pear-shaped balloon inflated from the apex to the base of the left ventricle induced the highest (P varying from 0.042 to 0.01, compared to the remaining balloon shapes) systolic aortic pressure and flow (104.6 ± 4.5 mmHg and 77.9 ± 1.7 mg/kg/min, respectively). In conclusion, a pear shaped balloon, inflated to a volume equal to the LVEDV, from the apex to the base of the left ventricle, induced an optimal hemodynamic effect during LVBP.

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