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Protein Turnover in Compensated Chronic Aortic Regurgitation

Roderick K King, Norman M Magid, George Opio, Jeffrey S Borer · Cardiology · 2008

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 [3H]-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. Howeve

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