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2,3-Butanedione monoxime suppresses primarily total calcium handling in canine heart
1Department of Physiology II, Okayama University Medical School, Okayama, 700-8558 Japan.
Insights
2,3-butanedione monoxime (BDM) primarily suppresses total calcium handling, not crossbridge cycling, in canine hearts. This finding clarifies BDM's mechanism in cardiac function research.
Area of Science:
- Cardiovascular Physiology
- Biochemistry
Background:
- The precise mechanism by which 2,3-butanedione monoxime (BDM) affects cardiac function is debated.
- It is unclear whether BDM inhibits crossbridge cycling or calcium (Ca2+) handling in the heart.
Purpose of the Study:
- To investigate whether BDM primarily affects crossbridge cycling or total Ca2+ handling in blood-perfused canine hearts.
- To utilize an integrative method to assess myocardial Ca2+ handling and cardiac mechanoenergetics.
Main Methods:
- Analysis of cardiac mechanoenergetics, including Emax (contractility), PVA (total mechanical energy), and O2 consumption in BDM-treated canine hearts.
- Determination of the internal Ca2+ recirculation fraction using postextrasystolic potentiation.
- Application of a novel integrative method to assess myocardial total Ca2+ handling.
Main Results:
- BDM treatment led to significant reductions in the internal Ca2+ recirculation fraction.
- Total Ca2+ handling in the BDM-treated hearts was significantly decreased.
- The reactivity of Emax to total Ca2+ handling remained largely unchanged.
Conclusions:
- BDM predominantly suppresses total Ca2+ handling rather than crossbridge cycling in the canine blood-perfused heart.
- The findings support BDM's role as an inhibitor of Ca2+ handling mechanisms in cardiac research.
Abstract:
Whether 2,3-butanedione monoxime (BDM, < or = 5mmol/l) suppresses primarily crossbridge cycling or total Ca(2+) handling in the blood-perfused whole heart remains controversial. Although BDM seems to suppress primarily total Ca(2+) handling in canine hearts, more evidence is lacking. We therefore analyzed the cardiac mechanoenergetics, namely, E(max) (contractility), PVA (total mechanical energy), and O(2) consumption of canine BDM-treated hearts by our recently developed integrative method to assess myocardial total Ca(2+) handling. This method additionally required the internal Ca(2+) 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 Ca(2+) recirculation fraction and total Ca(2+) handling in the BDM-treated heart, but virtually no change in the reactivity of E(max) to total Ca(2+) handling. This result corroborates the view that BDM suppresses primarily total Ca(2+) handling rather than crossbridge cycling in the canine blood-perfused heart.
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