Protein turnover in the in vitro perfused working rat heart.
We have examined the effects of various interventions on protein degradation and synthesis in the in vitro left side perfused working rat heart preparation of Taegtmeyer, Hems and Krebs. In the absence of insulin, we could not detect any effects of increased pressure workload or of increased volume workload on protein degradation. In the presence of insulin, increased pressure workload may inhibit protein degradation by about 30%. Hypoxia did not inhibit protein degradation when cardiac output was not deleteriously affected even though lactate output was greatly increased. A trebling of left atrial filling pressure stimulated protein synthesis in the left atrium by about 30%. This effect was observed when protein synthesis was expressed either relative to protein or relative to RNA. Right atrial protein synthesis was unaffected by the increased left atrial filling pressure and could be used as an internal control. We suggest that this acute effect of filling pressure on left atrial protein synthesis may be important in the development of left atrial hypertrophy which can occur in conditions where raised left atrial pressures are encountered, for example, in mitral stenosis.
D000818:Animals; D001011:Aorta / Q000502:physiology; D016275:Atrial Function; D001794:Blood Pressure; D002302:Cardiac Output; D006332:Cardiomegaly / Q000209:etiology; D003326:Coronary Circulation; D006321:Heart / Q000502:physiology*; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism; D010477:Perfusion; D011506:Proteins / Q000378:metabolism*; D012313:RNA / Q000378:metabolism; D051381:Rats
D007773:Lactates; D011506:Proteins; D019344:Lactic Acid; D012313:RNA; D010100:Oxygen