Abstract

BackgroundDiabetes 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.MethodsWe 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).ResultsWe 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.ConclusionsDiabetes 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.

Highlights

  • Diabetes is known to alter the energy metabolism of the heart

  • We show that the efficiencyafterload relation allows reconciliation of the conflicting conclusions in the literature regarding the effect of diabetes on myocardial efficiency

  • Streptozotocin-induced diabetes limits the ability of the heart to pump at high afterloads

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Summary

Introduction

Diabetes is known to alter the energy metabolism of the heart. it may be expected to affect the efficiency of contraction (i.e., the ratio of mechanical work output to metabolic energy input). 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. Some studies have reported an unchanged value in diabetic animals [6,7,8,9] We propose that these conflicting findings are a consequence of. For the first case (Figure 1A), compared with the control heart, the diabetic heart has a lower value of peak efficiency, but the same optimal afterload and the same peak afterload. If measurements had been made at or around the optimal afterload (the third case), one would find that the diabetic heart has the same efficiency as the control heart

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