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We studied hearts in which hypertrophy was caused by both pressure and volume overload. Pressure hypertrophy was induced by an aortic constriction; volume hypertrophy was induced by an iron-copper deficiency (anemia). The ventricular weight was increased by 34% in the pressure-hypertrophied hearts at the end of 6 weeks. The ventricular weight was increased by 54% in the volume-hypertrophied hearts at the end of 3 months. A potassium arrest-formalin fixation technique was used to produce a "diastole-like" ventricle. In the pressure-hypertrophied ventricle, the ventricular wall thickness and external radii were significantly increased, whereas the valve-to-apex distance and internal radii remained unchanged. We also found that in the volume-hypertrophied ventricle there was an increase in the valve-to-apex distance, external radii, internal radii, and wall thickness. Although external and internal dimensions increased, the ventricular shape did not change significantly in the volume-hypertrophied ventricle.
H L Lin, and
K V Katele, and
A F Grimm
January 1967,
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H L Lin, and
K V Katele, and
A F Grimm
January 2010,
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H L Lin, and
K V Katele, and
A F Grimm
February 1976,
Zeitschrift fur Kardiologie,
H L Lin, and
K V Katele, and
A F Grimm
August 1974,
Circulation research,
H L Lin, and
K V Katele, and
A F Grimm
October 1993,
FEBS letters,
H L Lin, and
K V Katele, and
A F Grimm
January 1987,
General pharmacology,
H L Lin, and
K V Katele, and
A F Grimm
October 1992,
Molecular and cellular biochemistry,
H L Lin, and
K V Katele, and
A F Grimm
October 1969,
Cardiovascular research,
H L Lin, and
K V Katele, and
A F Grimm
July 1997,
Circulation,
H L Lin, and
K V Katele, and
A F Grimm
February 1992,
Japanese circulation journal,
