Association of Cardiac Ventricular Myosin Isoforms with Hemodynamic Factors1

2015 ◽  
pp. 162-170
Author(s):  
C. D. Ianuzzo ◽  
B. Li ◽  
N. Hamilton ◽  
L. D�Costa ◽  
S. E. Ianuzzo ◽  
...  
Keyword(s):  
Myosin Isoforms ◽  
Ventricular Myosin

Myocardial biochemical and hemodynamic adaptations to chronic tachycardia

1991 ◽  
Vol 70 (2) ◽  
pp. 907-913 ◽  
Author(s):  
C. D. Ianuzzo ◽  
S. Brotherton ◽  
P. O'Brien ◽  
T. Salerno ◽  
M. H. Laughlin
Keyword(s):  
Blood Flow ◽  
Citrate Synthase ◽  
Left Ventricular ◽  
Myosin Isoforms ◽  
Cardiac Pacemakers ◽  
Tissue Samples ◽  
Ventricular Myosin ◽  
Yorkshire Pigs ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Biochemical Analyses

The purpose was to determine the biochemical and hemodynamic adaptations of the myocardium to chronic tachycardia. Cardiac pacemakers were implanted in Yorkshire pigs and set at a rate of 180 beats/min for a period of 35-42 days. Animals were then anesthetized with pentobarbital sodium. Myocardial blood flow and hemodynamics were determined at three different heart rates (i.e., 120, 180, and 220 beats/min). Tissue samples were then taken for microsphere and biochemical analyses. Chronically paced hearts maintained better cardiac function and had consistently higher left ventricular blood flow with a higher endocardial-to-epicardial ratio. The activities of citrate synthase and 3-hydroxyacyl-CoA dehydrogenase were 23 and 45% greater in the paced hearts, respectively. The sarcoplasmic reticulum adenosinetriphosphatase activity was 55% greater in the paced hearts, whereas the myosin adenosinetriphosphatase was the same as in the control hearts. Polyacrylamide gels of the ventricular myosin isoforms showed only the V3 type to be present in both the control and paced hearts. These findings show that the heart of a large mammal adapts to chronic tachycardia (i.e., 180 beats/min) by elevating the aerobic and calcium-sequestering capacities without altering its myosin type.

EFFECT OF AGING AND OBESITY ON VENTRICULAR MYOSIN ISOFORMS AND ENZYME ACTIVITIES 1011

1996 ◽  
Vol 28 (Supplement) ◽  
pp. 170
Author(s):  
H. A. Demirel ◽  
S. K. Powers ◽  
G. Farkas ◽  
J. Coombes ◽  
C. Caillaud ◽  
...  
Keyword(s):  
Enzyme Activities ◽  
Myosin Isoforms ◽  
Ventricular Myosin

scholarly journals Molecular cloning and characterization of human atrial and ventricular myosin alkali light chain cDNA clones.

1988 ◽  
Vol 263 (27) ◽  
pp. 13930-13936
Author(s):  
M Kurabayashi ◽  
I Komuro ◽  
H Tsuchimochi ◽  
F Takaku ◽  
Y Yazaki
Keyword(s):  
Molecular Cloning ◽  
Light Chain ◽  
Cdna Clones ◽  
Ventricular Myosin

Muscular myosin isoforms of (Cestoda)

2004 ◽  
Vol 28 (12) ◽  
pp. 885-894 ◽  
Author(s):  
L GONZALEZMALERVA ◽  
M CRUZRIVERA ◽  
O REYNOSODUCOING ◽  
C RETAMAL ◽  
A FLISSER ◽  
...  
Keyword(s):  
Myosin Isoforms

Electrophoretic Separation of Ventricular Myosin Isoenzymes Using a Native Polyacrylamide Minigel System

2003 ◽  
Vol 38 (1) ◽  
pp. 33-40 ◽  
Author(s):  
S. C. Garcia Pomblum ◽  
V. J. Pomblum ◽  
E. Gams ◽  
P. J. Reiser ◽  
J. D. Schipke
Keyword(s):  
Electrophoretic Separation ◽  
Myosin Isoenzymes ◽  
Ventricular Myosin

A treadmill exercise regimen for identifying cardiovascular phenotypes in transgenic mice

1997 ◽  
Vol 273 (3) ◽  
pp. H1595-H1605 ◽  
Author(s):  
J. G. Fewell ◽  
H. Osinska ◽  
R. Klevitsky ◽  
W. Ng ◽  
G. Sfyris ◽  
...  
Keyword(s):  
Treadmill Exercise ◽  
Genetic Manipulation ◽  
Ultrastructural Examination ◽  
Exercise Protocol ◽  
Hypertrophic Response ◽  
Cardiovascular Stress ◽  
Exercise Regimen ◽  
Ventricular Myosin ◽  
Tubular System ◽  
Transverse Axial

Cardiovascular stress in response to treadmill exercise is frequently used to detect cardiac abnormalities that are not readily apparent at rest. Herein we describe a treadmill exercise protocol for mice that allows for quantitation of the performance of an animal and the ability to gather metabolic information in a nonrestraining manner using telemetry implant devices. Transgenic (TG) mice overexpressing ventricular myosin regulatory light chain (MLC2v) were subjected to a 5-wk exercise regimen. The TG mice had significant decreases in their capacity for exercise at relatively high treadmill speeds compared with their nontransgenic (NTG) littermates. There was no indication of a hypertrophic response occurring in TG or NTG animals in response to the exercise protocol, and exercise had no effect on MLC2v phosphorylation. Ultrastructural examination of TG atria showed overtly normal myofibrillar organization but a proliferation of the transverse-axial tubular system. This exercise protocol should prove useful in detecting subtle phenotypes that occur in mice as a result of genetic manipulation of the cardiac compartment.

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