Effect of intraventricular pressure on protein synthesis in arrested rat hearts.
A modification of the Langendorff technique for perfusion of rat hearts was developed to allow a constant intraventricular pressure to be imposed on the left ventricle of arrested-catheterized hearts. This model was used to assess effects of increased aortic (60 and 120 mmHg) and intraventricular (0 and 25 mmHg) pressures on the rate of protein synthesis between 70 and 130 min of perfusion and on contents of ATP and creatine phosphate (creatine-P) in ventricles. Rates of protein synthesis in atria also were measured. Increased intraventricular or aortic pressure elevated the rate of protein synthesis (41%) compared with hearts supplied an aortic pressure of 60 mmHg and an intraventricular pressure of 0 mmHg. Higher intraventricular pressure also decreased the ribosomal subunit content. No change in the rate of protein synthesis was observed when intraventricular pressure was raised in hearts supplied an aortic pressure of 120 mmHg. Rates of atrial protein synthesis and contents of ATP and creatine-P were unchanged by elevations of either intraventricular or aortic pressure. These experiments indicate that stretch of the ventricular wall due to higher intraventricular or aortic pressure accelerated protein synthesis by maintaining the in vivo balance between rates of peptide chain initiation and elongation.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D006324:Heart Arrest, Induced; D006352:Heart Ventricles; D008297:Male; D009124:Muscle Proteins / Q000096:biosynthesis*; D009206:Myocardium / Q000378:metabolism*; D010441:Peptide Chain Elongation, Translational; D010442:Peptide Chain Initiation, Translational; D010477:Perfusion; D010725:Phosphocreatine / Q000378:metabolism; D011312:Pressure; D051381:Rats; D011919:Rats, Inbred Strains
D009124:Muscle Proteins; D010725:Phosphocreatine; D000255:Adenosine Triphosphate