Comparison of effects of dobutamine and ouabain on left ventricular contraction and relaxation in closed-chest dogs.

Abstract

Left ventricular (LV)' systole can be divided into phases: isovolumic contraction, ejection, end-systole, and isovolumic relaxation (1). Indices have been developed that describe LV performance during each of these four phases. However, it has been difficult to provide a description of the LV that spans all four phases, unifying and relating the various measures of LV performance. One possibility is to consider that LV systolic pumping function can be described as a time-varying elastance (2-5). In this concept, the LV is considered to behave as an elastic structure that stiffens in a predictable manner during systole. The LV pressure, P(t), at any time after the onset of contraction, t, is described by: P(t) = E(t) [V(t) -V0], where E(t) is LV elastance at t, V(t) the LV volume at t, and V0 the minimum volume required for the LV to generate super-atmospheric pressure. LV elastance, E(t), reaches a maximum value, E., at time t.,,, which has been termed end-systole. Ema,31which is the slope of the end-systolic pressure (PEs)-volume (VEs) relation, is a measure ofthe global inotropic state of the LV and is relatively insensitive to changes in loading conditions in isolated canine hearts (2, 3, 5-10), conscious dogs (1 1), and man (12, 13). Inotropic stimulation with catecholamines increases Emax and decreases t., the time from enddiastole to end-systole (2-4).In addition to the PES VEs relation, the time-varying elastance model has other implications that suggest links between the four phases ofsystole. For example, the model suggests that the maximum rate of rise of LV pressure (dP/dt4,), normally occurring during isovolumic contraction, is linearly related to the LV end-diastolic volume (VED) (3,4). The slope of this relation, dE/dtm., is also predicted to be sensitive to inotropic state and proportional to Ema/tm., providing a link between events occurring during isovolumic contraction and at endsystole. Further consideration of the time-varying elastance hypothesis (Appendix) also suggests that the rate of LV pressure fall during isovolumic relaxation should be inversely proportional to tm.. These predictions of the time-varying elastance model linking events occurring during isovolumic contraction (dP/dtm.,-VED relation), at end-systole (the PES-VES relation and tma), and during isovolumic relaxation (T) suggest that this model may provide a unified description of LV performance throughout systole.1. Abbreviations used in this paper: dE/dt., slope of dP/dtm,.-end-diastolic volume relation; dP/dtma, maximum rate of rise of P(t); ED, end-diastolic; Em,,t, slope ofend-systolic pressure-volume relation; ES, end-systolic; LV, left ventricular; P(t), LV pressure; t,,,, time from end-diastole to end-systole.Effect ofDobutamine and Ouabain 613 J. Clin. Invest.

Control of In Vivo Contraction/Relaxation Kinetics by Myosin Binding Protein C

“…Cardiac inotropes can differentially impact early (eg, dP/dt max ) versus late (eg, E es ) ejection-phase contractile parameters, with those working via PKA stimulation enhancing both, and those independent of PKA often having greater effects on the latter. 37 Our results support a greater role of PKA-phosphorylation of cMyBP-C in releasing its constraint over early contraction kinetics. This would also explain why dP/dt max -EDV relations were reduced more in cMyBP-C AllP-:(t/t) hearts than those lacking cMyBP-C entirely.…”

Assessment of the Temporal Relationship Between Left Ventricular Relaxation and Filling During Early Diastole Using Pulsed Doppler Echocardiography and Tissue Doppler Imaging

“…Therefore, the decrease in LV end-systolic volume due to an increase in myocardial contraction causes a rapid decline in LV pressure during isovolumic diastole, resulting in higher suction from the left atrium to the LV, induced by myocardial elastic recoil in this period. [22][23][24] Therefore, the LV wall expansion caused by elastic recoil during early diastole promotes LV filling, but the temporal relationship between the LV wall motion and the blood flow from the left atrium to the LV during this period has not been clarified.…”

Ventricular–vascular coupling in hypertension

“…80 The main limitation of this approach is related to left ventricular elastance calculation, which needs acute modifications of left ventricular load. 81 Considering negligible the value of V 0 (the theoretical ventricular volume at zero pressure), ventricular elastance has been estimated from a single beat 58,67,73,82,83 without considering V 0 . The assumption of V 0 equal to 'zero' substantially reduces the E lv and the ratio E a /E lv to a function of the ejection fraction [E a /E lv ¼ (1/LVEF) À 1] 84 and could lead to the wrong assumption that ejection fraction and E lv are interchangeable in this analysis (LVEF¼ Left Ventricular Ejection Fraction).…”