Ejecting activation differs in energetics from ordinary positive inotropism in the canine left ventricle.

Ventricular ejection is known to have dual effects on the end-systolic pressure: the ejecting deactivation by a relatively large ejection against a low afterload versus the ejecting activation by a relatively small ejection against a high afterload. We studied how the increase in contractility index (Emax) by the ejecting activation would affect myocardial oxygen consumption (VO2). To this end, left ventricular steady-state ejecting contractions were produced with various stroke volumes from a fixed end-diastolic volume in an excised cross-circulated canine heart. The effect of the ejection-activated Emax on VO2 was assessed by the relation between VO2 and pressure-volume area (PVA). PVA is the total mechanical energy generated by ventricular contraction. In contrast to the elevation of the linear VO2-PVA relation in a parallel manner with an enhanced Emax by ordinary positive inotropic agents such as catecholamines and calcium, the ejection-activated Emax did not elevate the VO2-PVA relation. This result indicates that the ejecting activation enhances Emax in an energetically different manner from ordinary positive inotropism in the canine left ventricle.