Diabetes is known to alter the energy metabolism of the heart. Thus, it may be expected to affect the efficiency of contraction (i.e ., the ratio of mechanical work output to metabolic energy input).
The literature on the subject is conflicting. The majority of studies have reported a reduction of myocardial efficiency of the diabetic heart, yet a number of studies have returned a null effect.
We propose that these discrepant findings can be reconciled by examining the dependence of myocardial efficiency on afterload.
Methods:
We performed experiments on streptozotocin (STZ)-induced diabetic rats (7-8 weeks post-induction), subjecting their (isolated) hearts to a wide range of afterloads (40 mmHg to maximal, where aortic flow approached zero). We measured work output and oxygen consumption, and their suitably scaled ratio (i.e ., myocardial efficiency).
Results:
We found that myocardial efficiency is a complex function of afterload: its value peaks in the mid-range and decreases on either side.
Diabetes reduced the maximal afterload to which the hearts could pump (105 mmHg versus 150 mmHg). Thus, at high afterloads (for example, 90 mmHg), the efficiency of the STZ heart was lower than that of the healthy heart (10.4% versus 14.5%) due to its decreased work output.
Diabetes also reduced the afterload at which peak efficiency occurred (optimal afterload: 63 mmHg versus 83 mmHg). Despite these negative effects, the peak value of myocardial efficiency (14.7%) was unaffected by diabetes.
Conclusions:
Diabetes reduces the ability of the heart to pump at high afterloads and, consequently, reduces the afterload at which peak efficiency occurs.
However, the peak efficiency of the isolated working rat heart remains unaffected by STZ-induced diabetes.
Author: June-Chiew HanSoyeon GooCarolyn J BarrettKimberley MellorAndrew J TabernerDenis S Loiselle
Credits/Source: Cardiovascular Diabetology 2014, 13:4
Published on: 2014-01-05
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