Relevance of the volume‐axis intercept, V0, compared with the slope of end‐systolic pressure–volume relationship in response to large variations in inotropy and afterload in rats

The end‐systolic pressure–volume relationship (ESPVR) is proposed and used as a reliable index of left ventricular (LV) contractility despite the fact that its afterload independence has been challenged. Furthermore, the physiological relevance of its volume‐axis intercept, V0, remains unclear. Systemic haemodynamics and pressure–volume loops obtained by inferior vena cava occlusion were recorded in 21 rats anaesthetized by isoflurane inhalation and instrumented with a conductance pressure–volume catheter in response to incremental i.v. doses of adrenaline, dobutamine, phenylephrine, metoprolol, papaverine and isoflurane inhalation. In conditions with large variations (±100%) of both inotropy and afterload, infusion of negative inotropic drugs was associated with a dose‐dependent rightward shift of ESPVR accompanied by a decrease in its slope (end‐systolic elastance, Ees), whereas positive inotropic agents produced an isolated decrease in V0. With the predominant vasoactive drugs, there was a dose‐dependent change in Ees without major horizontal shifts, demonstrating that this slope mainly represents LV afterload rather than inotropy. When contractility was altered, V0 was negatively correlated to the preload‐adjusted contractility index, PAdP/dtmax, demonstrating that a reduced V0 provides a good reflection of increased LV contractility. From these results, we computed a logarithmically adjusted Ees/V0 ratio, which resulted in reasonably strong concordance with PAdP/dtmax, including all the investigated drugs and dosages [n= 288; bias, 0.8 ± 16.2% (SD)]. Concordance with Ees (bias, 7.2 ± 58.7%) or V0 (bias, −0.6 ± 33.4%), used alone or with other commonly used contractility indices, was far less significant. In contrast to Ees, V0 provides a relatively good LV contractility index because it is much less sensitive to afterload.