Myofibrillar creatine kinase and cardiac contraction

1994 ◽  
Vol 133-134 (1) ◽  
pp. 125-144 ◽  
Author(s):  
Rene� Ventura-Clapier ◽  
Vladimir Veksler ◽  
Jacqueline A. Hoerter
Keyword(s):  
Creatine Kinase ◽  
Cardiac Contraction

Myofibrillar creatine kinase and cardiac contraction

1994 ◽  
pp. 125-144
Author(s):  
Reneé Ventura-Clapier ◽  
Vladimir Veksler ◽  
Jacqueline A. Hoerter
Keyword(s):  
Creatine Kinase ◽  
Cardiac Contraction

Reversible MM-creatine kinase binding to cardiac myofibrils

1987 ◽  
Vol 253 (3) ◽  
pp. C444-C455 ◽  
Author(s):  
R. Ventura-Clapier ◽  
V. A. Saks ◽  
G. Vassort ◽  
C. Lauer ◽  
G. V. Elizarova
Keyword(s):  
Creatine Kinase ◽  
Energy Supply ◽  
Adenine Nucleotides ◽  
Cardiac Contraction ◽  
Tension Development ◽  
Tension Recovery ◽  
Maximal Tension ◽  
Km Value ◽  
Rigor Tension ◽  
Length Changes

Skinned rat papillary muscles and purified preparations of rat cardiac myofibrils were used to study the nature of the interaction of creatine kinase with cardiac myofibrils. High activity of creatine kinase (2 IU/mg protein in fibers and 0.9 IU/mg in purified myofibrils) was due mostly to reversibly bound enzyme. This activity could be removed and rebound. The process of creatine kinase rebinding was characterized by apparent Km value of 0.14 mg/ml (approximately equal to 2 X 10(6) M). Rebinding of creatine kinase to cardiac myofibrils restored the phenomenon of functional compartmentation of adenine nucleotides in myofibrillar space and restored the ability of phosphocreatine to decrease the rigor tension in the presence of MgADP. The physiological experiments with quick length changes showed that rebinding of creatine kinase to skinned papillary muscle also restored Ca sensitivity, increased maximal tension development, decreased stiffness, and restored the tension recovery after quick length changes in muscle under condition of inhibition of endogenous creatine kinase by 1-fluoro-2,4-dinitrobenzene. It is concluded that creatine kinase reversibly bound to cardiac myofibrils is involved in the energy supply for cardiac contraction.

Ultrastructural alterations in the fetal mouse myocardium in response to genetic and environmental factors

1987 ◽  
Vol 45 ◽  
pp. 724-725
Author(s):  
K.C. Feng-Chen ◽  
F.B. Essien ◽  
K.J. Prestwidge ◽  
J.T. Cheng ◽  
C.L. Shen
Keyword(s):  
Fetal Heart ◽  
Perinatal Period ◽  
Primary Energy ◽  
Cardiac Contraction ◽  
Ultrastructural Changes ◽  
Fetal Mouse ◽  
The Subject ◽  
Physiological Adjustments ◽  
Genetic And Environmental Factors ◽  
Genetically Determined

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.

99mTc-Aminohexylidendiphosphonate and 99mTc-Pyrophos phate in the Scintigraphic Diagnosis of Experimental Cardiomyopathy in Dogs

1987 ◽  
Vol 26 (05) ◽  
pp. 220-223 ◽  
Author(s):  
L. Hadaš ◽  
J. VižĎa ◽  
P. Kafka ◽  
Y. Mazurová ◽  
V. Palicka ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Plasma Levels ◽  
Maximum Accumulation ◽  
Kinase A ◽  
Good Agreement

Experimental cardiomyopathy was provoked in 24 dogs with high intravenous doses of adrenaline and theophylline. These lesions were studied by means of the new agent 99mTc-AHDP and 99mTc-PYP in comparison. Cardiomyopathy could be imaged as early as 4 h after the onset of involvement but not later than 7 days. A maximum accumulation occurred in lesions 24 h old. 99mTc uptake in the myocardium was graded scintigraphically. 99mTc-AHDP was accumulated in the altered’myocardium to a greater extent than 99mTc-PYP. Scintigraphic findings were in good agreement with plasma levels of creatine- kinase. A comparison with histology demonstrated that the maximum accumulation of radiopharmaceuticals occurred at the time when the development of myocardium involvement reached the stage of myocytolysis.

Human creatine kinase: Isoenzymes and logistics of energy distribution

1984 ◽  
Vol 44 (7) ◽  
pp. 611-615 ◽  
Author(s):  
Christer Sylvén ◽  
Eva Jansson ◽  
Anders Kallner ◽  
Kim Böök
Keyword(s):  
Creatine Kinase ◽  
Energy Distribution ◽  
Creatine Kinase Isoenzymes

HEART COMPLICATIONS IN HYPERTHYROIDISM

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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