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Cardiac dysfunction in aging conscious rats: altered cardiac cytoskeletal proteins as a potential mechanism

¹Cardiovascular Research Institute and Department of Cell Biology & Molecular Medicine, University of Medicine & Dentistry of New Jersey, New Jersey Medical School, Newark; and ²Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, New Jersey

Submitted 11 February 2008 ; accepted in final form 27 May 2008

The objective of this study was to test the hypothesis that the mechanism mediating left ventricular (LV) dysfunction in the aging rat heart involves, in part, changes in cardiac cytoskeletal components. Our results show that there were no significant differences in heart rate, LV pressure, or LV diameter between conscious, instrumented young [5.9 ± 0.3 mo (n = 9)] and old rats [30.6 ± 0.1 mo (n = 10)]. However, the first derivative of LV pressure (LV dP/dt) was reduced (8,309 ± 790 vs. 11,106 ± 555 mmHg/s, P < 0.05) and isovolumic relaxation time () was increased (8.7 ± 0.7 vs. 6.3 ± 0.6 ms, P < 0.05) in old vs. young rats, respectively. The differences in baseline LV function in young and old rats, which were modest, were accentuated after β-adrenergic receptor stimulation with dobutamine (20 µg/kg), which increased LV dP/dt by 170 ± 9% in young rats, significantly more (P < 0.05) than observed in old rats (115 ± 5%). Volume loading in anesthetized rats demonstrated significantly impaired LV compliance in old rats, as measured by the LV end-diastolic pressure and dimension relationship. In old rat hearts, there was a significant (P < 0.05) increase in the percentage of LV collagen (2.4 ± 0.2 vs. 1.3 ± 0.2%), -tubulin (92%), and β-tubulin (2.3-fold), whereas intact desmin decreased by 51%. Thus the cardiomyopathy of aging in old, conscious rats may be due not only to increases in collagen but also to alterations in cytoskeletal proteins.

aging cardiomyopathy; left ventricular systolic function; left ventricular diastolic function; tubulin