Endothelin and Cardiac Contraction

The physiology of the fetal heart differs significantly from that of the mature post-natal organ: e.g., the metabolic supply for adult cardiac contraction relies mainly on fatty acids; whereas, the fetal heart uses carbohydrates as its primary energy source. Limited morphological descriptions of the developing myocardium have appeared. However, additional studies are required to elucidate the ultrastructural changes occuring in the perinatal period when enormous physiological adjustments are made. Although adult animals are most often used in toxocological and pathological analyses, it is also important to investigate fetal cardiac responsiveness to various agents. The vulnerability of the ultrastructure of the fetal mouse myocardium to genetic and environmental assault is the subject of this report. The genetically determined effect on the heart was observed in mouse embryos homozygous for the cab (cardiac abnormality) mutation discovered by Essien.

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HEART COMPLICATIONS IN HYPERTHYROIDISM

Journal of Medicine and Pharmacy ◽

10.34071/jmp.2011.2.1 ◽

2011 ◽

pp. 7-17

Author(s):

Hai Thuy Nguyen ◽

Anh Vu Nguyen

Keyword(s):

Atrial Fibrillation ◽

Blood Pressure ◽

Heart Rate ◽

Heart Diseases ◽

Systolic Dysfunction ◽

Oxygen Demand ◽

Left Ventricular ◽

Cardiac Contraction ◽

Cardiac Complications ◽

Cardiac Symptoms

Thyroid hormone increases the force of the contraction and the amount of the heart muscle oxygen demand. It also increases the heart rate. Due to these reasons, the work of the heart is greatly increased in hyperthyroidism. Hyperthyroidism increases the amount of nitric oxide in the intima, lead them to be dilated and become less stiff. Cardiac symptoms can be seen in anybody with hyperthyroidism, but can be particularly dangerous in whom have underlying heart diseases. Common symptoms include: tachycardia and palpitations. Occult hyperthyroidism is a common cause of an increased heart rate at rest and with mild exertion. Hyperthyroidism can also produce a host of other arrhythmias such as PVCs, ventricular tachycardia and especially atrial fibrillation. Left ventricular diastolic dysfunction and systolic dysfunction, Mitral regurgitation and mitral valve prolapsed are heart complications of hyperthyroism could be detected by echocardiography. The forceful cardiac contraction increases the systolic blood pressure despite the increased relaxation in the blood vessels reduces the diastolic blood pressure. Atrial fibrillation, atrial enlargement and congestive heart failure are important cardiac complications of hyperthyroidism. An increased risks of stroke is common in patients with atrial fibrillation. Graves disease is linked to autoimmune complications, such as cardiac valve involvement, pulmonary arterial hypertension and specific cardiomyopathy. Worsening angina: Patients with coronary artery disease often experience a marked worsening in symptoms with hyperthyroidism. These can include an increase in chest pain (angina) or even a heart attack.

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Faculty Opinions recommendation of On the geometrical relationship between global longitudinal strain and ejection fraction in the evaluation of cardiac contraction.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718268201.793516963 ◽

2016 ◽

Author(s):

Jens-Uwe Voigt

Keyword(s):

Ejection Fraction ◽

Longitudinal Strain ◽

Global Longitudinal Strain ◽

Cardiac Contraction ◽

Geometrical Relationship

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NOS1, S-nitrosylation and cardiac contraction

10.36866/pn.82.36 ◽

2011 ◽

pp. 36-38

Author(s):

Honglan Wang ◽

Mark Ziolo

Keyword(s):

Cardiac Contraction

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Evaluation of Ca2+ compartments responsible for cardiac contraction in guinea pig papillary muscle

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)44696-9 ◽

1997 ◽

Vol 73 ◽

pp. 47

Author(s):

Shigeki Miyamoto ◽

Hiroshi Ozaki ◽

Masatoshi Hori ◽

Masao Endoh ◽

Hideaki Karaki

Keyword(s):

Guinea Pig ◽

Papillary Muscle ◽

Cardiac Contraction

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The lapse of cardiac contraction as affected by intrathoracic function

American Heart Journal ◽

10.1016/s0002-8703(37)90930-x ◽

1937 ◽

Vol 13 (1) ◽

pp. 120-121

Author(s):

J.M.S.

Keyword(s):

Cardiac Contraction

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Homocyst(e)ine impairs endocardial endothelial function

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y99-102 ◽

1999 ◽

Vol 77 (12) ◽

pp. 950-957 ◽

Cited By ~ 26

Author(s):

Suresh C Tyagi ◽

Lane M Smiley ◽

Vibhas S Mujumdar

Keyword(s):

Nitric Oxide ◽

Methyl Ester ◽

Cardiac Function ◽

Vascular Function ◽

Ex Vivo ◽

Cardiac Contraction ◽

Normal Male ◽

Wistar Kyoto ◽

Endocardial Endothelium ◽

Endothelial Nitric Oxide

Homocyst(e)ine injured vascular endothelium and modulated endothelial-dependent vascular function. Endothelium plays an analogous role in both the vessel and the endocardium. Therefore, we hypothesized that homocyst(e)ine modulated endocardial endothelium (EE) dependent cardiac function. The ex vivo cardiac rings from normal male Wistar-Kyoto rats were prepared. The contractile responses of left and right ventricular rings were measured in an isometric myobath, using different concentrations of CaCl2. The response was higher in the left ventricle than right ventricle and was elevated in endocardium without endothelium. The half effective concentration (EC50) and maximum tension generated by homocyst(e)ine were 106 and 5-fold lower than endothelin (ET) and angiotensin II (AII), respectively. However, in endothelial-denuded endocardium, homocyst(e)ine response was significantly increased (p < 0.005, compared with intact endothelium) and equal to the response to ET and AII. To determine the physiological significance of ET, AII, homocyst(e)ine, and endothelial nitric oxide in EE function, cardiac rings were pretreated with AII (10-10 M) or ET (10-13 M) and then treated with homocyst(e)ine (10-8 M). Results suggested that at these concentrations AII, ET, or homocyst(e)ine alone had no effect on cardiac contraction. However, in the presence of 10-10 M AII or 10-13 M ET, the cardiac contraction to homocyst(e)ine (10-8 M) was significantly enhanced (p < 0.01, compared with without pretreatment) and further increased in the endocardium without endothelium. The pretreatment of cardiac ring with the inhibitor of nitric oxide, Nω-nitro-L-arginine methyl ester (L-NAME), increased contractile response to homocyst(e)ine. These results suggested that homocyst(e)ine impaired EE-dependent cardiac function and acted synergistically with AII and ET in enhancing the cardiac contraction.Key words: endocardial remodeling, homocyst(e)ine, contraction, endothelin, angiotensin, endothelial-derived relaxing factor (EDRF), Nω-nitro-L-arginine methyl ester (L-NAME), endothelial dysfunction, ex vivo cardiac function, heart failure.

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Phosphorylation of cardiac myosin binding protein C releases myosin heads from the surface of cardiac thick filaments

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1614020114 ◽

2017 ◽

Vol 114 (8) ◽

pp. E1355-E1364 ◽

Cited By ~ 35

Author(s):

Robert W. Kensler ◽

Roger Craig ◽

Richard L. Moss

Keyword(s):

Protein C ◽

Structural Changes ◽

Binding Protein ◽

Cardiac Contraction ◽

Cardiac Myosin ◽

Cross Bridge ◽

Myosin Binding Protein ◽

Myosin Binding Protein C ◽

Thick Filaments ◽

Myosin Binding

Cardiac myosin binding protein C (cMyBP-C) has a key regulatory role in cardiac contraction, but the mechanism by which changes in phosphorylation of cMyBP-C accelerate cross-bridge kinetics remains unknown. In this study, we isolated thick filaments from the hearts of mice in which the three serine residues (Ser273, Ser282, and Ser302) that are phosphorylated by protein kinase A in the m-domain of cMyBP-C were replaced by either alanine or aspartic acid, mimicking the fully nonphosphorylated and the fully phosphorylated state of cMyBP-C, respectively. We found that thick filaments from the cMyBP-C phospho-deficient hearts had highly ordered cross-bridge arrays, whereas the filaments from the cMyBP-C phospho-mimetic hearts showed a strong tendency toward disorder. Our results support the hypothesis that dephosphorylation of cMyBP-C promotes or stabilizes the relaxed/superrelaxed quasi-helical ordering of the myosin heads on the filament surface, whereas phosphorylation weakens this stabilization and binding of the heads to the backbone. Such structural changes would modulate the probability of myosin binding to actin and could help explain the acceleration of cross-bridge interactions with actin when cMyBP-C is phosphorylated because of, for example, activation of β1-adrenergic receptors in myocardium.

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Analysis of Passive Filling With Fibrotic Myocardial Infarction

Volume 3: Biomedical and Biotechnology Engineering ◽

10.1115/imece2015-50003 ◽

2015 ◽

Cited By ~ 1

Author(s):

Fulufhelo Masithulela

Keyword(s):

Myocardial Infarction ◽

Structural Changes ◽

Strain Energy Function ◽

Transversely Isotropic ◽

Magnetic Resonance Images ◽

Cardiac Contraction ◽

Diastolic Filling ◽

Element Analysis ◽

Infarcted Heart ◽

Longitudinal Strains

Cardiovascular diseases account for one third of all deaths worldwide, more than 33% of which are related to ischemic heart disease, involving a myocardial infarction (MI). Following myocardial infarction, the injured region and ventricle undergo structural changes which are thought to be caused by elevated stresses and reduction of strains in the infarcted wall. The fibrotic phase is defined as the period when the amount of new collagen and number of fibroblasts rapidly increase in the infarcted tissue. We studied through finite element analysis the mechanics of the infarcted and remodeling rat heart during diastolic filling. Biventricular geometries of healthy and infarcted rat hearts reconstructed from magnetic resonance images were imported in Abaqus©. The passive myocardium was modelled as a nearly incompressible, hyperelastic, transversely isotropic material represented by the strain energy function W = ½C(eQ − 1) with Q = bfE112 + bt(E222 + E332 + E322) + bfs(E122 + E212 + E132 + E312). Material parameters were obtained from literature [1]. As boundary conditions, the circumferential and longitudinal displacements at the base were set to zero. The radial displacements at the base were left free. A linearly increasing pressure from 0 to 3.80 kPa and 0.86 kPa, respectively, was applied to the endocardial surfaces of left and right ventricle. Average radial, circumferential and longitudinal strains during passive filling were −0.331, 0.135, 0.042 and −0.250, −0.078 and 0.046 for the healthy heart and the infarcted heart, respectively. The average radial, circumferential and longitudinal stresses were −1.196 kPa, 3.87 kPa in the healthy heart and 0.424 kPa and −1.90 kPa, 8.74 kPa and 1.69 kPa in the infarcted heart. The strains were considerable lower in the infarcted heart compared to the health heart whereas stresses were higher in the presence of an infarct compared to the healthy case. The results of this study indicate the feasibility of the models developed for a more comprehensive assessment of mechanics of the infarcted ventricle including extension to account for cardiac contraction.

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