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Preload does not influence nonmechanical O2 consumption in isolated rabbit heart
A Higashiyama1, M W Watkins, Z Chen
1Cardiology Unit, College of Medicine, University of Vermont, Burlington 05405.
The American Journal of Physiology
|March 1, 1994
Summary
Left ventricular diastolic volume does not significantly impact myocardial nonmechanical energy consumption in rabbit hearts. This suggests length-dependent activation in the whole heart does not incur an energetic cost.
Area of Science:
- Cardiology
- Physiology
- Biochemistry
Background:
- Myocardial nonmechanical activity, crucial for excitation-contraction coupling, exhibits length dependence in isolated muscle studies.
- Previous whole-heart studies suggested minimal preload effects on nonmechanical energy consumption.
- Unloaded oxygen consumption (VO2) may inaccurately estimate nonmechanical VO2 due to residual cross-bridge cycling.
Purpose of the Study:
- To accurately quantify the influence of left ventricular (LV) diastolic volume on nonmechanical VO2 in the whole heart.
- To investigate the energetic cost of length-dependent activation in the intact heart.
Main Methods:
- Utilized 2,3-butanedione monoxime (BDM) to quantify nonmechanical VO2 in excised rabbit ventricles.
- Measured VO2 and force-time integral under high (VH) and low (VL) LV volumes.
- Estimated nonmechanical VO2 as the VO2-axis intercept of the VO2-force-time integral relationship during BDM infusion.
Main Results:
- Nonmechanical VO2 did not significantly differ between high and low LV volumes (P = 0.702).
- Multiple linear regression analysis confirmed no significant effect of LV diastolic volume on nonmechanical VO2 (P = 0.361).
- Physiological ranges of LV end-diastolic pressure were maintained.
Conclusions:
- Left ventricular diastolic volume does not significantly affect nonmechanical energy consumption in the physiological range in rabbit hearts.
- Length-dependent activation does not appear to have an energetic cost in the whole rabbit heart.
- The findings suggest increased Ca2+ affinity for contractile proteins is the primary mechanism for length-dependent activation.