Whether 2,3-butanedione monoxime (BDM, less than or equal to5 mmol/l) suppr
esses primarily crossbridge cycling or total Ca2+ handling in the blood-per
fused whole heart remains controversial. Although BDM seems to suppress pri
marily total Ca2+ handling in canine hearts, more evidence is lacking. We t
herefore analyzed the cardiac mechanoenergetics, namely, E-max (contractili
ty), PVA (total mechanical energy), and O-2 consumption of canine BDM-treat
ed hearts by our recently developed integrative method to assess myocardial
total Ca2+ handling. This method additionally required the internal Ca2+ r
ecirculation fraction. We obtained this from the beat constant of the expon
ential decay component of the postextrasystolic potentiation. Our analysis
indicated significant decreases in both internal Ca2+ recirculation fractio
n and total Ca2+ handling in the BDM-treated heart, but virtually no change
in the reactivity of E-max to total Ca2+ handling. This result corroborate
s the view that BDM suppresses primarily total Ca2+ handling rather than cr
ossbridge cycling in the canine blood-perfused heart.