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  • Title: Pressure versus flow stress: the response of cardiac protein synthesis.
    Author: Schreiber SS, Oratz M, Rothschild MA.
    Journal: Recent Adv Stud Cardiac Struct Metab; 1975; 8():397-412. PubMed ID: 1215644.
    Abstract:
    Cardiac stress produced by hypertension or excess volume loading results in different types of hypertrophy. Elevated left ventricular pressure rapidly results in increased myocardial protein synthesis in vivo and in vitro, but such rapid alterations are not consistently seen in volume loading. The difference in response is difficult to clarify since it is not possible to effect alterations in left ventricular pressure or perfusion without profoundly affecting coronary perfusion. The present study describes cardiac protein synthesis in the right ventricle of the young guinea pig heart in vitro utilizing a perfusion model in which the right ventricle could be stressed by elevations of pressure or volume loading in the presence of constant and restricted coronary perfusion. With coronary flow maintained at 25 ml/min/g dry wt, an increase in right ventricular pressure from normal levels of 3 mm Hg to 11 mm Hg resulted in a 60% increase of myocardial incorporation of lysine-14 C into protein. However, with further increases of right ventricular pressure to 22 mm Hg, protein synthesis dropped back to normal levels. The fall-off in protein synthesis was not due to decreased contractility, alterations in intracellular lysine pool specific activity, or alterations in total coronary flow or pressure. A 60% increase in coronary perfusion was associated with a similar response of protein synthesis to progressive elevations of pressure. Since the ATP levels rose and lactate production fell, a deficiency of O2 did not entirely explain the decline of protein synthesis with maximal pressures. At all levels of coronary perfusion, volume loading for 3 hr did not result in increased protein incorporation of lysine-14 C. The studies indicate a relationship between ventricular pressure and protein synthesis unrelated to coronary flow per se and suggest a pressure receptor triggering protein synthesis within the ventricular wall. Such a relationship is not apparent in short term volume loading in vitro.
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