Cardiac function and morphology with aging in the spontaneously hypertensive rat

1979 ◽  
Vol 237 (4) ◽  
pp. H461-H468 ◽  
Author(s):  
J. M. Pfeffer ◽  
M. A. Pfeffer ◽  
M. C. Fishbein ◽  
E. D. Frohlich
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Stroke Volume ◽  
Right Ventricle ◽  
Cardiac Function ◽  
Spontaneously Hypertensive Rat ◽  
Left Ventricular ◽  
Ether Anesthesia ◽  
Spontaneously Hypertensive ◽  
The Right

To determine the effects of a chronic pressure load on cardiac function and morphology, spontaneously hypertensive rats (SHR) and two normotensive strains of Wistar rats (WKY and NWR) were studied under ether anesthesia at 13, 25, 52, and 90 wk of age. Although resting cardiac index of the SHR was comparable to that of WKY and NWR at all ages, the peak cardiac output and peak stroke volume per gram of left ventricle determined during a rapid intravenous infusion of Tyrode solution was markedly reduced in the SHR only at 90 wk of age. Autonomic inhibition did not alter the peak stroke volume attained, but reduced peak cardiac output at all ages in each of the strains. Absolute left ventricular dimensions in the SHR increased out of proportion to body growth, consistent with concentric hypertrophy. As peak pumping ability markedly declined from 52 to 90 wk of age in the SHR, the free wall of the left ventricle greatly thickened whereas the septum remained unchanged. At this time the right ventricle also hypertrophied. This disproportionate thickening of the walls of the left ventricle and the hypertrophy of the right ventricle were reflected in measurements of their fiber diameters. These alterations in ventricular architecture may contribute to the decrease in pumping ability observed in long-standing hypertension.

scholarly journals Synergy in the heart: RV systolic function plays a key role in optimizing LV performance during exercise

2020 ◽  
Vol 319 (3) ◽  
pp. H642-H650
Author(s):  
B. Ruijsink ◽  
M. N. Velasco Forte ◽  
P. Duong ◽  
L. Asner ◽  
K. Pushparajah ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Right Ventricle ◽  
Cardiac Function ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Systolic Function ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Exact Role ◽  
The Right

The right ventricle appears to have an important impact on maintaining systemic cardiac function and delivering stroke volume. However, its exact role in supporting left ventricular function has so far been unclear. This study demonstrates a new mechanism of ventricular interaction that provides mechanistic understanding of the key importance of the right ventricle in driving cardiac performance.

Concomitant Pulsatile and Continuous Flow VAD in Biventricular and Univentricular Physiology: A Comparison Study with a Numerical Model

2017 ◽  
Vol 40 (2) ◽  
pp. 74-81 ◽  
Author(s):  
Arianna Di Molfetta ◽  
Gianfranco Ferrari ◽  
Roberta Iacobelli ◽  
Sergio Filippelli ◽  
Paolo Guccione ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Numerical Model ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Continuous Flow ◽  
Single Ventricle ◽  
Left Ventricular ◽  
Ventricular Assist Devices ◽  
Fontan Physiology ◽  
The Right

Introduction To develop and test a lumped parameter model to simulate and compare the effects of the simultaneous use of continuous flow (CF) and pulsatile flow (PF) ventricular assist devices (VADs) to assist biventricular circulation vs. single ventricle circulation in pediatrics. Methods Baseline data of 5 patients with biventricular circulation eligible for LVAD and of 5 patients with Fontan physiology were retrospectively collected and used to simulate patient baselines. Then, for each patient the following simulations were performed: (a) CF VAD to assist the left ventricle (single ventricle) + a PF VAD to assist the right ventricle (cavo-pulmonary connection) (LCF + RPF); (b) PF VAD to assist the left ventricle (single ventricle) + a CF VAD to assist the right ventricle (cavo-pulmonary connection) (RCF + LPF) Results In biventricular circulation, the following results were found: cardiac output (17% RCF + LPF, 21% LCF + RPF), artero-ventricular coupling (-36% for the left ventricle and -21.6% for the right ventricle), pulsatility index (+6.4% RCF + LPF, p = 0.02; -8.5% LCF + RPF, p = 0.00009). Right (left) atrial pressure and right (left) ventricular volumes are decreased by the RCF + LPF (by RPF + LCF). Pulmonary arterial pressure decreases in the LCF + RPF configuration. In Fontan physiology: cardiac output (LCF + RPF 35% vs. 8% in RCF + LPF), ventricular preload (+4% RCF + LPF, -10% LCF + RPF), Fontan conduit pressure (-5% RCF + LPF, +7% LCF + RPF), artero-ventricular coupling (-14% RCF + LPF vs. -41% LCF + RPF) and pulsatility (+13% RCF + LPF, - 8% LCF + RPF). Conclusions A numerical model supports clinicians in defining and innovating the VAD implantation strategy to maximize the hemodynamic benefits. Results suggest that the hemodynamic benefits are maximized by the LCF + RPF configuration.

Regulation of K+ and Ca2+ channels in experimental cardiac failure

1991 ◽  
Vol 261 (6) ◽  
pp. H1979-H1987 ◽  
Author(s):  
M. Gopalakrishnan ◽  
D. J. Triggle ◽  
A. Rutledge ◽  
Y. W. Kwon ◽  
J. A. Bauer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Cardiac Failure ◽  
Radioligand Binding ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
The Right

To examine the status of ATP-sensitive K+ (K+ATP) channels and 1,4-dihydropyridine-sensitive Ca2+ (Ca2+DHP) channels during experimental cardiac failure, we have measured the radioligand binding properties of [3H]glyburide and [3H]PN 200 110, respectively, in tissue homogenates from the rat cardiac left ventricle, right ventricle, and brain 4 wk after myocardial infarction induced by left coronary artery ligation. The maximal values (Bmax) for [3H]glyburide and [3H]PN 200 110 binding were reduced by 39 and 40%, respectively, in the left ventricle, and these reductions showed a good correlation with the right ventricle-to-body weight ratio in heart-failure rats. The ligand binding affinities were not altered. In the hypertrophied right ventricle, Bmax values for both the ligands were not significantly different when data were normalized to DNA content or right ventricle weights but showed an apparent reduction when normalized to unit protein or tissue weight. Moderate reductions in channel densities were observed also in whole brain homogenates from heart failure rats. Assessment of muscarinic receptors, beta-adrenoceptors and alpha 1-adrenoceptors by [3H]quinuclidinyl benzilate, [3H]dihydroalprenolol, and [3H]prazosin showed reductions in left ventricular muscarinic and beta-adrenoceptor densities but not in alpha 1-adrenoceptor densities, consistent with earlier observations. It is suggested that these changes may in part contribute to the pathology of cardiac failure.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

In the Loop—Left Ventricular Pressures

2011 ◽  
pp. 42-47
Author(s):  
James R. Munis
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Aortic Valve ◽  
Left Ventricle ◽  
Stroke Volume ◽  
Cardiovascular System ◽  
Aortic Root ◽  
Left Ventricular ◽  
Root Pressure ◽  
The Third

We've already looked at 2 types of pressure that affect physiology (atmospheric and hydrostatic pressure). Now let's consider the third: vascular pressures that result from mechanical events in the cardiovascular system. As you already know, cardiac output can be defined as the product of heart rate times stroke volume. Heart rate is self-explanatory. Stroke volume is determined by 3 factors—preload, afterload, and inotropy—and these determinants are in turn dependent on how the left ventricle handles pressure. In a pressure-volume loop, ‘afterload’ is represented by the pressure at the end of isovolumic contraction—just when the aortic valve opens (because the ventricular pressure is now higher than aortic root pressure). These loops not only are straightforward but are easier to construct just by thinking them through, rather than by memorization.

scholarly journals Genomic modulation of mitochondrial respiratory genes in the hypertrophied heart reflects adaptive changes in mitochondrial and contractile function

2007 ◽  
Vol 293 (5) ◽  
pp. H2819-H2825 ◽  
Author(s):  
Makhosazane Zungu ◽  
Maria Pilar Alcolea ◽  
Francisco José García-Palmer ◽  
Martin E. Young ◽  
M. Faadiel Essop
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Respiratory Function ◽  
Hypobaric Hypoxia ◽  
Contractile Function ◽  
Left Ventricular ◽  
Transcript Levels ◽  
Mitochondrial Number ◽  
The Right ◽  
Mitochondrial Respiratory

We hypothesized the coordinate induction of mitochondrial regulatory genes in the hypertrophied right ventricle to sustain mitochondrial respiratory capacity and contractile function in response to increased load. Wistar rats were exposed to hypobaric hypoxia (11% O2) or normoxia for 2 wk. Cardiac contractile and mitochondrial respiratory function were separately assessed for the right and left ventricles. Transcript levels of several mitochondrial regulators were measured. A robust hypertrophic response was observed in the right (but not left) ventricle in response to hypobaric hypoxia. Mitochondrial O2 consumption was increased in the right ventricle, while proton leak was reduced vs. normoxic controls. Citrate synthase activity and mitochondrial DNA content were significantly increased in the hypertrophied right ventricle, suggesting higher mitochondrial number. Transcript levels of nuclear respiratory factor-1, peroxisome proliferator-activated receptor-γ-coactivator-1α, cytochrome oxidase (COX) subunit II, and uncoupling protein-2 (UCP2) were coordinately induced in the hypertrophied right ventricle following hypoxia. UCP3 transcript levels were significantly reduced in the hypertrophied right ventricle vs. normoxic controls. Exposure to chronic hypobaric hypoxia had no significant effects on left ventricular mitochondrial respiration or contractile function. However, COXIV and UCP2 gene expression were increased in the left ventricle in response to chronic hypobaric hypoxia. In summary, we found coordinate induction of several genes regulating mitochondrial function and higher mitochondrial number in a model of physiological right ventricular hypertrophy, linking the efficiency of mitochondrial oxidative phosphorylation and respiratory function to sustained contractile function in response to the increased load.

Delayed enhancement imaging in a contemporary patient cohort following correction of tetralogy of Fallot

2014 ◽  
Vol 25 (7) ◽  
pp. 1268-1275 ◽  
Author(s):  
Uta Preim ◽  
Philipp Sommer ◽  
Janine Hoffmann ◽  
Jana Kehrmann ◽  
Lukas Lehmkuhl ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Tetralogy Of Fallot ◽  
Nyha Class ◽  
Left Ventricular ◽  
Delayed Enhancement ◽  
Volume Index ◽  
Delayed Enhancement Imaging ◽  
The Right ◽  
Myocardial Scars

AbstractObjectiveTo test the hypothesis that myocardial scars after repair of tetralogy of Fallot are related to impaired cardiac function and adverse clinical outcome.MethodsA total of 53 patients were retrospectively analysed after repair of tetralogy of Fallot. The median patient age was 20 years (range 2–48).Cardiac MRI with a 1.5 T magnet included cine sequences to obtain volumes and function, phase-sensitive inversion recovery delayed enhancement imaging to detect myocardial scars, and flow measurements to determine pulmonary regurgitation fraction. In addition, clinical parameters were obtained.ResultsAn overall 83% of patients were in NYHA class I. All patients with the exception of 2 (96%) had pulmonary insufficiency. Mean ejection fraction and end-diastolic volume index were 46% and 128 ml/m2 for the right ventricle and 54% and 82 ml/m2 for the left ventricle, respectively. Excluding enhancement of the septal insertion and prosthetic patches, delayed enhancement was seen in 11/53 cases (21%). Delayed enhancement of the right ventricle was detected in 6/53 patients (11%) and of the left ventricle in 5/53 patients (9%). The patient group with delayed enhancement was significantly older (p=0.003), had later repair (p=0.007), and higher left ventricular myocardial mass index (p=0.009) compared with the group without delayed enhancement.ConclusionsThis study reveals that scarring is common in patients after surgical repair of tetralogy of Fallot and is associated with older age and late repair. However, there was no difference in right ventricular function, NYHA class, or occurrence of clinically relevant arrhythmias between patients with and those without myocardial scars.

scholarly journals Epigenetics, inflammation and metabolism in right heart failure associated with pulmonary hypertension

2017 ◽  
Vol 7 (3) ◽  
pp. 572-587 ◽  
Author(s):  
Nolwenn Samson ◽  
Roxane Paulin
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pressure Overload ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Ventricular Failure ◽  
Pulmonary Arterial ◽  
Ventricle Hypertrophy ◽  
The Right

Right ventricular failure (RVF) is the most important prognostic factor for both morbidity and mortality in pulmonary arterial hypertension (PAH), but also occurs in numerous other common diseases and conditions, including left ventricle dysfunction. RVF remains understudied compared with left ventricular failure (LVF). However, right and left ventricles have many differences at the morphological level or the embryologic origin, and respond differently to pressure overload. Therefore, knowledge from the left ventricle cannot be extrapolated to the right ventricle. Few studies have focused on the right ventricle and have permitted to increase our knowledge on the right ventricular-specific mechanisms driving decompensation. Here we review basic principles such as mechanisms accounting for right ventricle hypertrophy, dysfunction, and transition toward failure, with a focus on epigenetics, inflammatory, and metabolic processes.

Myocardial function in rat genetic models of low and high aerobic running capacity

2002 ◽  
Vol 282 (3) ◽  
pp. R721-R726 ◽  
Author(s):  
John C. Barbato ◽  
Soon Jin Lee ◽  
Lauren Gerard Koch ◽  
George T. Cicila
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Cardiac Function ◽  
Atp Hydrolysis ◽  
Mrna Level ◽  
Inbred Strains ◽  
Left Ventricular ◽  
Genetic Models ◽  
Heart Preparation ◽  
The Mean

We recently evaluated treadmill aerobic running capacity in 11 inbred strains of rats and found that isolated working left ventricular function correlated ( r = 0.86) with aerobic running capacity. Among these 11 strains the Buffalo (BUF) hearts produced the lowest and the DA hearts the highest isolated cardiac output. The goal of this study was to investigate the components of cardiac function (i.e., coronary flow, heart rates, stroke volume, contractile dynamics, and cross-bridge cycling) to characterize further the BUF and DA inbred strains as potential models of contrasting myocardial performance. Cardiac performance was assessed using the Langendorff-Neely working heart preparation. Isolated DA hearts were superior ( P< 0.05) to the BUF hearts for cardiac output (63%), stroke volume (60%), aortic +dP/d t (47%), and aortic −dP/d t(46%). The mean α/β-myosin heavy chain (MHC) isoform ratio for DA hearts was 21-fold higher relative to BUF hearts. At the steady-state mRNA level, DA hearts had a fivefold higher α/β-ratio than the BUF hearts. The mean rate of ATP hydrolysis by MHCs was 64% greater in DA compared with BUF ventricles. These data demonstrate that the BUF and DA strains can serve as genetic models of contrasting low and high cardiac function.

Alterations in ventricular excitability in conscious dogs during development of chronic heart failure

1986 ◽  
Vol 250 (6) ◽  
pp. H1022-H1029 ◽  
Author(s):  
C. W. White ◽  
M. J. Mirro ◽  
D. D. Lund ◽  
D. J. Skorton ◽  
N. G. Pandian ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Time Course ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Maximum Increase ◽  
Electrophysiological Properties ◽  
Cycle Lengths ◽  
The Right

Arrhythmias in patients with heart failure may result from altered electrophysiological properties of the myocardium. To examine changes in ventricular excitability during cardiac failure and to relate these changes to ventricular structural and neurochemical abnormalities, right ventricular failure was produced in dogs by pulmonary artery banding and by creating tricuspid regurgitation. Right and left ventricular excitability thresholds were tested biweekly in heart failure (HF) and sham-operated conscious dogs by means of strength-duration curves (1-40 ms) at basic cycle lengths (BCL) of 300-500 ms until time of death (21-188 days). Marked increases in the excitability threshold of the right ventricle occurred in HF (mean maximum % increase, 205 +/- 42 at BCL 500 ms). Smaller, though significant increases in the left ventricular excitability threshold in HF were also seen (mean maximum % increase 103 +/- 36 at BCL 500 ms). Increases in the excitability threshold of the left as well as the right ventricles occurred, even though ventricular dilation (2-D Echo) was confined to the right ventricle. The time course of changes in the excitability threshold was variable (maximum occurrence at 21 +/- 3 days right ventricle, 23 +/- 11 days left ventricle). Tyrosine hydroxylase activity and norepinephrine content of the right ventricle were markedly depleted at death, when the excitability threshold was high. Similar though nonsignificant trends in reductions of these sympathetic neurochemicals were seen in the left ventricle. Levels of choline acetyltransferase and QNB binding in both ventricles were unaffected.

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