title: Energy metabolism after ischemic preconditioning in streptozotocin-induced diabetic rat hearts.
abstract: OBJECTIVE
  The aim of this study was to compare the cardioprotective effects of preconditioning in hearts from streptozotocin-induced diabetic rats with its effects in normal rat hearts.
  
  
  BACKGROUND
  The protective effect of ischemic preconditioning against myocardial ischemia may come from improved energy balance. However, it is not known whether preconditioning can also afford protection to diabetic hearts.
  
  
  METHODS
  Isolated perfused rat hearts were either subjected (preconditioned group) or not subjected (control group) to preconditioning before 30 min of sustained ischemia and 30 min of reperfusion. Preconditioning was achieved with two cycles of 5 min of ischemia followed by 5 min of reperfusion.
  
  
  RESULTS
  In the preconditioned groups of both normal and diabetic rats, left ventricular developed pressure, high energy phosphates, mitochondrial adenosine triphosphatase and adenine nucleotide translocase activities were significantly preserved after ischemia-reperfusion; cumulative creatine kinase release was smaller during reperfusion; and myocardial lactate content was significantly lower after sustained ischemia. However, cumulative creatine kinase release was less in the preconditioned group of diabetic rats than in the preconditioned group of normal rats. Under ischemic conditions, more glycolytic metabolites were produced in the diabetic rats (control group) than in the normal rats, and preconditioning inhibited these metabolic changes to a similar extent in both groups.
  
  
  CONCLUSIONS
  The present study demonstrates that in both normal and diabetic rats, preservation of mitochondrial oxidative phosphorylation and inhibition of glycolysis during ischemia can contribute to preconditioning-induced cardioprotection. Furthermore, our data suggest that diabetic myocardium may benefit more from preconditioning than normal myocardium, possibly as a result of the reduced production of glycolytic metabolites during sustained ischemia and the concomitant attenuation of intracellular acidosis.
authors.affiliation: Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan. tatsumi@koto.kpu-m.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Tatsumi
authors.forename: S
authors.initials: S
authors.lastname: Matoba
authors.forename: M
authors.initials: M
authors.lastname: Kobara
authors.forename: N
authors.initials: N
authors.lastname: Keira
authors.forename: A
authors.initials: A
authors.lastname: Kawahara
authors.forename: K
authors.initials: K
authors.lastname: Tsuruyama
authors.forename: T
authors.initials: T
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Katamura
authors.forename: C
authors.initials: C
authors.lastname: Nakagawa
authors.forename: B
authors.initials: B
authors.lastname: Ohta
authors.forename: Y
authors.initials: Y
authors.lastname: Yamahara
authors.forename: J
authors.initials: J
authors.lastname: Asayama
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D003401:Creatine / Q000378:metabolism; D003402:Creatine Kinase / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology / Q000378:metabolism*; D004734:Energy Metabolism; D006003:Glycogen / Q000378:metabolism; D066298:In Vitro Techniques; D019157:Ischemic Preconditioning, Myocardial; D019344:Lactic Acid / Q000378:metabolism; D008929:Mitochondria, Heart / Q000201:enzymology; D009206:Myocardium / Q000737:chemistry / Q000201:enzymology / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D000227:Adenine Nucleotides; D010725:Phosphocreatine; D019344:Lactic Acid; D006003:Glycogen; D003402:Creatine Kinase; D003401:Creatine