|ELSHERIF, LAILA - UNIV OF LOUISVILLE
|ORTINES, RAYMOND - UNIV OF LOUISVILLE
|KANG, Y - UNIV OF LOUISVILLE
Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/2/2002
Publication Date: 3/14/2003
Citation: Elsherif, L., Ortines, R., Saari, J.T., Kang, Y.J. 2003. Hypertrophy and heart failure in a mouse model of copper deficiency [abstract]. The Federation of American Societies for Experimental Biology Journal. 17:A1128.
Technical Abstract: Dietary copper deficiency (CuD) leads to hypertrophic cardiomyopathy in various experimental models. Various aspects of this hypertrophy have been under investigation for a long time. However, the transition from compensated hypertrophy to decompensated heart failure has not been investigated in the study of CuD. We set out to investigate the contractile and hemodynamic parameters of the CuD mouse heart and to determine whether heart failure follows hypertrophy in CuD. Dams of FVB mice were fed CuD or copper-adequate (CuA) diet starting from the third day post delivery and the weanling pups were fed the same diet for a total period of 5 wks. At wk 4, female mice were used for the analysis of heart functional parameters using a surgical technique for catheterizing the left ventricle. A significant decrease in left ventricle systolic pressure was observed with no change in heart rate, and more importantly contractility, as measured by the maximal rate of left ventricular pressure rise (+dP/dt), was significantly depressed in the CuD mice. On the other hand, left ventricle end-diastolic pressure was elevated, and relaxation was impaired in the CuD animals. In addition to changes in the basal level of cardiac function, CuD hearts had a blunted response to the beta-adrenergic agonist isoproterenol. This study shows that CuD leads to systolic and diastolic dysfunction, which are indices commonly used to diagnose heart failure. Supported in part by NIH grant HL63760.