Short-term anoxia does not impair protein turnover in isolated perfused turtle heart

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Protein turnover was studied under conditions of normoxia and anoxia in isolated perfused turtle (Trachemys (=Pseudemys) scripta elegans) hearts at 15 °C. Protein synthesis was measured by 3H-labelled phenylalanine incorporation into the protein pool. Protein degradation was studied using the protein synthesis inhibitor cycloheximide and measuring phenylalanine release from the heart. Heart rate, cardiac output and ventricle pressure development were unaffected by 2 h of anoxia. Protein synthesis rate was tenfold lower in turtle heart than in rat heart at their respective body temperatures. However, 1 h of anoxia did not affect the rate of protein synthesis in turle heat. RNA content of both ventricle and atria decreased after anoxic perfusion. Protein synthesis rates in atria were higher than those of ventricle under conditions of either anoxia or normoxia. Protein degradation rate did not change in cycloheximide-treated turtle hearts after 2 h of anoxia. These findings indicate that lack of oxygen per se does not affect protein turnover in the isolated perfused turtle heart. This feature presumably allows protein turnover to proceed in vivo during routine dives at elevated temperatures. Also, the turtle heart is a good model system to study the effects of anoxia on protein turnover without the potentially confounding factor of contractile failure. These hearts are very resistant to anoxia and well able to maintain contractility for extended periods of time.