Key Points
- To determine whether ventricular loading conditions and regional functional nonuniformity influence the rate of left ventricular pressure fall through interdependent or separate mechanisms.
- Studied seven anesthetized dogs (N=7), altering ventricular loading conditions using vena cavae occlusions and intravenous dextran infusions.
- Induced regional nonuniformity by administering 8 to 20 ng of intracoronary isoproterenol into the left anterior descending artery, tracking anterior and posterior segment lengths via midwall sonomicrometers.
- Evaluated the rate of left ventricular pressure decay by measuring peak negative dP/dt, the relaxation time constant (tau), and isovolumic relaxation duration.
- Volume loading reduced the rate of left ventricular pressure fall without altering regional or temporal nonuniformity indexes.
- Intracoronary isoproterenol induced regional wall nonuniformity and slowed pressure decay without altering global loading conditions.
- The relaxation-slowing effect of isoproterenol remained consistent across different left ventricular volumes, confirming that loading and nonuniformity act via largely independent pathways.
Structured PICO
PPopulation7 anesthetized dogs
IInterventionAlteration of loading conditions (vena cavae occlusions and/or intravenous infusions of dextran) and induction of nonuniformity (intracoronary injection of 8-20 ng of isoproterenol into the mild left anterior descending coronary artery)
CComparatorBaseline or alternative loading/uniformity states
OOutcomeRate of left ventricular pressure fall (assessed with peak -dP/dt, time constant tau, and duration of isovolumic relaxation)surrogate
In the intact, ejecting left ventricle, loading conditions and nonuniformity are important and independent determinants of the rate of isovolumic relaxation.