Abstract
We have previously reported that high Ca2+ infusion produces a Ca2+-overloaded contractile failure in rat hearts associated with a parallel downward shift of the linear relation between left ventricular (LV) myocardial oxygen consumption per beat (VO2) and systolic pressure-volume area (PVA) (VO2-PVA relation), linking to proteolysis of a cytoskeletal protein, α-fodrin. We hypothesized that intracoronary infusion with a β-adrenergic receptor agonist, dobutamine causes a similar contractile failure after its clearance. To test this hypothesis, we investigated LV mechanical work and energetics in cross-circulated excised rat hearts. After control volume loading run (control vol-run), two different runs during dobutamine infusion were performed. After stopping dobutamine infusion, back control vol-run was performed. The curved LV end-systolic pressure-volume relation obtained in back control vol-run shifted downward from that in control vol-run. The VO2-PVA relation also shifted downward; the VO2 intercept significantly decreased (n=7). In these hearts, we found a proteolysis of α-fodrin in the hearts underwent intracoronary infusion with dobutamine. The result indicated that LV mechanical work and energetics were suppressed after clearance of dobutamine similar to high Ca2+, though they were enhanced during dobutamine infusion. The suppression on mechanoenergetics in these stunned hearts is linked to a proteolysis of α-fodrin as in Ca2+-overloaded contractile failing hearts. [Jpn J Physiol 54 Suppl:S102 (2004)]
