Key Points
- To assess the specific effects of elevated ventricular pressure and volume loading on right ventricular protein synthesis under controlled coronary perfusion.
- Perfused isolated young guinea pig hearts in vitro under constant and restricted coronary flow (4 ml/min per heart; 25 ml/min/g dry weight).
- Subjected the right ventricle to step increases in pressure (from 3 mm Hg to 11 and 22 mm Hg) or volume loading for 3 hours.
- Measured myocardial protein synthesis via [14C]lysine incorporation alongside metabolic markers including ATP, lactate, and coronary flow distribution.
- Increasing right ventricular pressure from 3 mm Hg to 11 mm Hg resulted in a 60 percent increase in myocardial [14C]lysine incorporation into protein.
- Further elevating right ventricular pressure to 22 mm Hg caused protein synthesis to decline back to normal baseline levels, which was not explained by contractility loss or oxygen deficiency despite increased ATP and reduced lactate.
- Volume loading for 3 hours failed to induce myocardial protein synthesis at any tested level of coronary perfusion.
Structured PICO
Does elevated right ventricular pressure or volume loading increase myocardial protein synthesis in isolated guinea pig hearts with constant coronary perfusion?
PPopulationYoung male guinea pigs (260-320 g, 4-6 weeks post-weaning) isolated heart perfusion model
IInterventionElevation of right ventricular pressure (to 11 mm Hg or 22 mm Hg) or volume loading for 3 hours with constant coronary perfusion
CComparatorNormal right ventricular pressure (3 mm Hg) or baseline volume loading
OOutcomeMyocardial incorporation of (14C)lysine into protein (protein synthesis)surrogate
Elevated right ventricular pressure initially stimulates myocardial protein synthesis independent of coronary flow, but this effect is lost at maximal pressures, suggesting a pressure receptor mechanism within the ventricular wall.