Key Points
- To evaluate how acute increases in left-atrial filling pressure affect left-atrial protein synthesis rates in an isolated, perfused working heart model.
- Perfused working rat hearts in vitro under controlled conditions using the Taegtmeyer working heart preparation.
- Held aortic pressure (afterload) constant at either 70 cmH2O or 100 cmH2O while increasing left-atrial filling pressure (preload) from baseline (5 or 7.5 cmH2O) up to 20 cmH2O.
- Measured left-atrial protein synthesis normalized to protein and RNA content, using right-atrial synthesis rates as an internal control.
- Increasing filling pressure from 5 to 20 cmH2O at an aortic pressure of 70 cmH2O, or from 7.5 to 20 cmH2O at an aortic pressure of 100 cmH2O, significantly stimulated left-atrial protein synthesis rates by 30% to 40%.
- Stimulation remained consistent when normalized to either protein or RNA content, while right-atrial protein synthesis rates remained unchanged and matched baseline left-atrial rates.
Structured PICO
PPopulationPerfused working rat heart preparation in vitro
IInterventionIncreased left-atrial filling pressure (from 5 to 20 cmH2O at aortic pressure 70 cmH2O, or 7.5 to 20 cmH2O at aortic pressure 100 cmH2O)
CComparatorLower filling pressures (5 or 7.5 cmH2O) and right-atrial protein synthesis (internal control)
OOutcomeRate of left-atrial protein synthesissurrogate
Acute increases in left-atrial filling pressure stimulate protein synthesis, suggesting a mechanism for the development of left-atrial hypertrophy in conditions with raised pulmonary venous pressures.