BACKGROUND: The controversially discussed intrinsic effect of end-diastolic pressure (EDP) on ventricular relaxation (lusitropy) is a prerequisite for interpretation of lusitropic changes induced by physiological and pharmacological interventions because the latter usually alter the ventricular loading conditions. OBJECTIVES: Characterization of the lusitropic effect of preload changes at low and high absolute EDP and after spontaneous cardiodepression. METHODS: Repeated preload tests (increasing cardiac inflow at constant mean aortic pressure) were performed in isolated ejecting rat and guinea pig hearts. Preload was quantified by left ventricular EDP, lusitropy was quantified using peak negative left ventricular pressure change velocity (-dP/dt), and relaxation time constant tau was calculated from monoexponential and four-parametric logistic pressure fall models. Regression coefficients of relaxation indexes, -dP/dt and tau versus EDP, were calculated and compared at different degrees of cardiac depression. RESULTS: Increasing EDP in the ejecting hearts less than 2 h after isolation caused tau to decrease and -dP/dt to increase initially at low EDP levels. Both parameters remained constant or even reversed at higher EDP levels. In the spontaneously depressed hearts, over 3 h after isolation, basic tau values were higher and -dP/dt values were lower, but EDP changes no longer had significant lusitropic effects. The same behaviour was observed in pentobarbital depressed hearts. CONCLUSIONS: A positive lusitropic effect (falling tau, rising -dP/dt) was observed when preload was increased in the range of lower EDP values in undepressed hearts early after isolation. However, preload changes did not influence lusitropy in isolated hearts either early after isolation at high EDP levels or in the spontaneously depressed condition at any EDP level.
BACKGROUND: The controversially discussed intrinsic effect of end-diastolic pressure (EDP) on ventricular relaxation (lusitropy) is a prerequisite for interpretation of lusitropic changes induced by physiological and pharmacological interventions because the latter usually alter the ventricular loading conditions. OBJECTIVES: Characterization of the lusitropic effect of preload changes at low and high absolute EDP and after spontaneous cardiodepression. METHODS: Repeated preload tests (increasing cardiac inflow at constant mean aortic pressure) were performed in isolated ejecting rat and guinea pig hearts. Preload was quantified by left ventricular EDP, lusitropy was quantified using peak negative left ventricular pressure change velocity (-dP/dt), and relaxation time constant tau was calculated from monoexponential and four-parametric logistic pressure fall models. Regression coefficients of relaxation indexes, -dP/dt and tau versus EDP, were calculated and compared at different degrees of cardiac depression. RESULTS: Increasing EDP in the ejecting hearts less than 2 h after isolation caused tau to decrease and -dP/dt to increase initially at low EDP levels. Both parameters remained constant or even reversed at higher EDP levels. In the spontaneously depressed hearts, over 3 h after isolation, basic tau values were higher and -dP/dt values were lower, but EDP changes no longer had significant lusitropic effects. The same behaviour was observed in pentobarbital depressed hearts. CONCLUSIONS: A positive lusitropic effect (falling tau, rising -dP/dt) was observed when preload was increased in the range of lower EDP values in undepressed hearts early after isolation. However, preload changes did not influence lusitropy in isolated hearts either early after isolation at high EDP levels or in the spontaneously depressed condition at any EDP level.
Authors: M Hori; M Inoue; M Fukunami; M Kitakaze; Y Ishida; K Tsujioka; S Nakajima; A Kitabatake; H Abe Journal: Cardiovasc Res Date: 1985-10 Impact factor: 10.787