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Am J Physiol Heart Circ Physiol 278: H1840-H1847, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 6, H1840-H1847, June 2000

Decreased passive stiffness of cardiac myocytes and cardiac tissue from copper-deficient rat hearts

Lois Jane Heller1, David E. Mohrman1, and Joseph R. Prohaska2

Departments of 1 Medical and Molecular Physiology and 2 Biochemistry and Molecular Biology, School of Medicine, University of Minnesota, Duluth, Duluth, Minnesota 55812

Passive stiffness characteristics of isolated cardiac myocytes, papillary muscles, and aortic strips from male Holtzman rats fed a copper-deficient diet for ~5 wk were compared with those of rats fed a copper-adequate diet to determine whether alterations in these characteristics might accompany the well-documented cardiac hypertrophy and high incidence of ventricular rupture characteristic of copper deficiency. Stiffness of isolated cardiac myocytes was assessed from measurements of cellular dimensional changes to varied osmotic conditions. Stiffness of papillary muscles and aortic strips was determined from resting length-tension analyses and included steady-state characteristics, dynamic viscoelastic stiffness properties, and maximum tensile strength. The primary findings were that copper deficiency resulted in cardiac hypertrophy with increased cardiac myocyte size and fragility, decreased cardiac myocyte stiffness, and decreased papillary muscle passive stiffness, dynamic stiffness, and tensile strength and no alteration in aortic connective tissue passive stiffness or tensile strength. These findings suggest that a reduction of cardiac myocyte stiffness and increased cellular fragility could contribute to the reduced overall cardiac tissue stiffness and the high incidence of ventricular aneurysm observed in copper-deficient rats.

cardiac hypertrophy; myocyte dimensions; papillary muscles; osmotic stress


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