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      Protein Turnover in Compensated Chronic Aortic Regurgitation

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          We recently demonstrated dynamic alterations in protein turnover 3 days and 1 month after surgical induction of aortic regurgitation (AR). To characterize protein synthesis and degradation during the long-term plateau phase, we performed [<sup>3</sup>H]-leucine infusion 2.5 years after induction of AR in 10 New Zealand White rabbits and 12 sham-operated controls. Protein fractional synthesis rates were obtained by analyses of plasma and protein hydrolysates, growth rates from protein concentration and heart weight measurements, and degradation rates by subtraction of growth from synthesis rates. AR (regurgitant fraction 25 ± 11%) caused a 57% increase in left ventricular (LV) weight in comparison with controls (7.4 ± 1.7 vs. 4.7 ± 0.6 g, p < 0.001) and no evidence of heart failure. Although concentrations of total cardiac protein, myosin heavy chain and actin were similar, the enlarged AR hearts had increased amounts of total cardiac protein (1,009 ± 312 vs. 682 ± 120mg/LV, p < 0.05), myosin heavy chain (148 ± 91 vs. 81 ± 29 mg/LV, p < 0.05), and actin (73 ± 42 vs. 44 ± 16 mg/LV, p < 0.06). Individual protein fractional synthesis and degradation rates were closely balanced. However, myosin fractional synthesis rates were 152% (p < 0.01) greater than those of total cardiac protein in AR animals, while only 52% (p < 0.05) greater in controls (AR vs. controls, p = 0.05). Variations in actin turnover between AR and control animals did not attain statistical significance. Myosin and actin fractional synthesis rates correlated closely in AR rabbits (R = 0.81 p < 0.02), but not among controls (R = 0.41, NS). Thus, selective alterations in myofibrillar protein turnover contribute to the maintenance of increased myofibrillar protein content in the ‘compensatory’ LV hypertrophy of chronic AR.

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          Author and article information

          S. Karger AG
          21 November 2008
          : 88
          : 6
          : 518-525
          Division of, Cardiovascular Pathophysiology, Cornell University Medical College, New York Hospital-Cornell Medical Center, New York, N.Y., USA
          177402 Cardiology 1997;88:518–525
          © 1997 S. Karger AG, Basel

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          Page count
          Pages: 8
          General Cardiology, Basic Science


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