Whether 2,3-butanedione monoxime (BDM, ≤5mmol/l) suppresses primarily crossbridge cycling or total Ca2+ handling in the blood-perfused whole heart remains controversial. Although BDM seems to suppress primarily total Ca2+ handling in canine hearts, more evidence is lacking. We therefore analyzed the cardiac mechanoenergetics, namely, Emax (contractility), PVA (total mechanical energy), and O2 consumption of canine BDM-treated hearts by our recently developed integrative method to assess myocardial total Ca2+ handling. This method additionally required the internal Ca2+ recirculation fraction. We obtained this from the beat constant of the exponential decay component of the postextrasystolic potentiation. Our analysis indicated significant decreases in both internal Ca2+ recirculation fraction and total Ca2+ handling in the BDM-treated heart, but virtually no change in the reactivity of Emax to total Ca2+ handling. This result corroborates the view that BDM suppresses primarily total Ca2+ handling rather than crossbridge cycling in the canine blood-perfused heart.
- Sarcoplasmic reticulum
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