title: Various models of cardiac conditioning in single or sequential periods of ischemia: comparative effects on infarct size and intracellular signaling.
abstract: BACKGROUND
  Preconditioning (PreC) and postconditioning (PostC) reduce infarct size. We sought to determine the effects of PreC and PostC, alone or in combination, on infarct size and expression of intracellular signals in different ischemia models.
  
  
  METHODS
  Male rabbits were subjected to myocardial ischemia followed by 3-hour reperfusion. In a first series we applied 3 ischemia models [a 20-min period (20), a 40-min period (40), and two sequential 20-min periods (20-20)] and 3 types of interventions [no intervention (controls, C), 2 cycles of 5-min ischemia/10-min reperfusion before index ischemia (PreC) and 6 cycles of 10-s ischemia/10-s reperfusion after index ischemia and/or between the sequential ischemic periods (PostC)] (12 groups in total). Infarct size (I) and area at risk (R) were assessed (%I/R). In a second series, samples were taken for western blot analysis of Akt phosphorylation.
  
  
  RESULTS
  Overall, %I/R differed significantly among groups (p<0.001). In control groups, C-40 had a greater %I/R than C-20 (p=0.006). In intervention groups, no differences were found in %I/R. All intervention groups had significantly lower %I/R compared to C-40 group (p<0.001), whereas, compared to C-20-20 group, PreC-20-20, 20-PostC-20, 20-PostC-20-PostC and PreC-20-20-PostC groups had lower %I/R (all p<0.05). Akt was increased in all groups in which a significant %I/R reduction was achieved (p<0.05 versus all other groups).
  
  
  CONCLUSIONS
  PreC and PostC, alone or in combination, are effective when an ischemic insult of a given duration is applied either as a single or as sequential periods. Protection from either intervention is associated with an enhanced Akt activation.
authors.affiliation: Second Department of Cardiology, University of Athens Medical School, Attikon University Hospital, Athens, Greece.
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Iliodromitis
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Farmakis
authors.forename: Ioanna
authors.initials: I
authors.lastname: Andreadou
authors.forename: Anastasia
authors.initials: A
authors.lastname: Zoga
authors.forename: Sofia-Iris
authors.initials: SI
authors.lastname: Bibli
authors.forename: Theodora
authors.initials: T
authors.lastname: Manolaki
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Dagres
authors.forename: Efstathios K
authors.initials: EK
authors.lastname: Iliodromitis
authors.forename: Maria
authors.initials: M
authors.lastname: Anastasiou-Nana
authors.forename: Dimitrios Th
authors.initials: DT
authors.lastname: Kremastinos
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D007424:Intracellular Fluid / Q000502:physiology*; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology* / Q000628:therapy*; D017202:Myocardial Ischemia / Q000473:pathology / Q000628:therapy; D011817:Rabbits; D011897:Random Allocation; D015398:Signal Transduction / Q000502:physiology*; D013997:Time Factors; D016896:Treatment Outcome