title: Streptozotocin-induced diabetes prolongs twitch duration without affecting the energetics of isolated ventricular trabeculae.
abstract: BACKGROUND
  Diabetes induces numerous electrical, ionic and biochemical defects in the heart. A general feature of diabetic myocardium is its low rate of activity, commonly characterised by prolonged twitch duration. This diabetes-induced mechanical change, however, seems to have no effect on contractile performance (i.e., force production) at the tissue level. Hence, we hypothesise that diabetes has no effect on either myocardial work output or heat production and, consequently, the dependence of myocardial efficiency on afterload of diabetic tissue is the same as that of healthy tissue.
  
  
  METHODS
  We used isolated left ventricular trabeculae (streptozotocin-induced diabetes versus control) as our experimental tissue preparations. We measured a number of indices of mechanical (stress production, twitch duration, extent of shortening, shortening velocity, shortening power, stiffness, and work output) and energetic (heat production, change of enthalpy, and efficiency) performance. We calculated efficiency as the ratio of work output to change of enthalpy (the sum of work and heat).
  
  
  RESULTS
  Consistent with literature results, we showed that peak twitch stress of diabetic tissue was normal despite suffering prolonged duration. We report, for the first time, the effect of diabetes on mechanoenergetic performance. We found that the indices of performance listed above were unaffected by diabetes. Hence, since neither work output nor change of enthalpy was affected, the efficiency-afterload relation of diabetic tissue was unaffected, as hypothesised.
  
  
  CONCLUSIONS
  Diabetes prolongs twitch duration without having an effect on work output or heat production, and hence efficiency, of isolated ventricular trabeculae. Collectively, our results, arising from isolated trabeculae, reconcile the discrepancy between the mechanical performance of the whole heart and its tissues.
authors.affiliation: Auckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand. j.han@auckland.ac.nz.
authors.forename: June-Chiew
authors.initials: JC
authors.lastname: Han
authors.forename: Kenneth
authors.initials: K
authors.lastname: Tran
authors.forename: Poul M F
authors.initials: PM
authors.lastname: Nielsen
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Taberner
authors.forename: Denis S
authors.initials: DS
authors.lastname: Loiselle
mesh_terms: D000818:Animals; D002151:Calorimetry / Q000379:methods; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology; D004734:Energy Metabolism / Q000502:physiology*; D006352:Heart Ventricles / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D009924:Organ Culture Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
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