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06:22
Contractility Measurements on Isolated Papillary Muscles for the Investigation of Cardiac Inotropy in Mice
Published on: September 17, 2015
2,3-Butanedione monoxime increases contractile efficiency in the rabbit ventricle
M W Watkins1, B K Slinker, Y Goto
1Department of Medicine, University of Vermont College of Medicine, Burlington 05405.
The American Journal of Physiology
|December 1, 1992
Summary
2,3-butanedione monoxime (BDM) increased left ventricular (LV) contractile efficiency by inhibiting cross-bridge formation. This study demonstrates BDM
Area of Science:
- Cardiovascular Physiology
- Biophysics
- Biochemistry
Background:
- Left ventricular (LV) contractile efficiency, a measure of chemomechanical energy transduction, is typically assessed via the pressure-volume area (PVA) and oxygen consumption (VO2).
- Previous interventions like adrenergic agents and calcium channel blockers have not altered contractile efficiency, but hyperthyroidism has been shown to decrease it.
- This decrease is hypothesized to stem from an increased V1/V3 myosin isoenzyme ratio, suggesting cross-bridge dynamics are key.
Purpose of the Study:
- To investigate if direct alteration of cross-bridge cycling affects LV contractile efficiency.
- To test the hypothesis that inhibiting cross-bridge formation with 2,3-butanedione monoxime (BDM) would change contractile efficiency.
Main Methods:
- Seven excised rabbit LVs were perfused with red blood cells and subjected to isovolumetric contractions.
- 2,3-butanedione monoxime (BDM), a negative inotropic agent, was administered at 3-4 mM perfusate concentration.
- Measurements included contractility (Emax), time to end systole (Tmax), relaxation half time (T1/2), LV oxygen consumption (VO2), and pressure-volume area (PVA).
Main Results:
- BDM reversibly decreased contractility (Emax) by 11% and shortened Tmax and T1/2.
- LV contractile efficiency significantly increased by approximately 27% (from 36.5% to 46.4%) due to a 20% decrease in the slope of the VO2-PVA relation.
- Oxygen costs of the mechanically unloaded LV decreased by 12%, and BDM also induced coronary vasodilation.
Conclusions:
- Direct inhibition of cross-bridge formation by BDM enhances LV contractile efficiency.
- This finding supports the hypothesis that cross-bridge cycling directly influences the efficiency of energy transduction in the heart.
- BDM's effects on contractile efficiency, mechanical function, and coronary vasodilation highlight its complex impact on cardiac performance.
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