title: Short-term diabetes attenuates left ventricular dysfunction and mortality rates after myocardial infarction in rodents.
abstract: OBJECTIVE
  To investigate the effects of hyperglycemia on left ventricular dysfunction, morphometry, myocardial infarction area, hemodynamic parameters, oxidative stress profile, and mortality rate in rats that had undergone seven days of myocardial infarction.
  
  
  BACKGROUND
  Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury.
  
  
  METHODS
  Male Wistar rats were divided into four groups: control-sham, diabetes-sham, myocardial infarction, and diabetes + myocardial infarction. Myocardial infarction was induced 14 days after diabetes induction. Ventricular function and morphometry, as well as oxidative stress and hemodynamic parameters, were evaluated after seven days of myocardial infarction.
  
  
  RESULTS
  The myocardial infarction area, which was similar in the infarcted groups at the initial evaluation, was reduced in the diabetes + myocardial infarction animals (23 ± 3%) when compared with the myocardial infarction (42 ± 7%, p < 0.001) animals at the final evaluation. The ejection fraction (22%, p = 0.003), velocity of circumferential fiber shortening (30%, p = 0.001), and left ventricular isovolumetric relaxation time (26%, p = 0.002) were increased in the diabetes + myocardial infarction group compared with the myocardial infarction group. The diabetes-sham and diabetes + myocardial infarction groups displayed increased catalase concentrations compared to the control-sham and myocardial infarction groups (diabetes-sham: 32 ± 3; diabetes + myocardial infarction: 35 ± 0.7; control-sham: 12 ± 2; myocardial infarction: 16 ± 0.1 pmol min⁻¹ mg⁻¹ protein). The levels of thiobarbituric acid-reactive substances were reduced in the diabetes-sham rats compared to the control-sham rats. These positive adaptations were reflected in a reduced mortality rate in the diabetes + myocardial infarction animals (18.5%) compared with the myocardial infarction animals (40.7%, p = 0.001).
  
  
  CONCLUSIONS
  These data suggest that short-term hyperglycemia initiates compensatory mechanisms, as demonstrated by increased catalase levels, which culminate in improvements in the ventricular response, infarcted area, and mortality rate in diabetic rats exposed to ischemic injury.
authors.affiliation: Human Movement Laboratory, São Judas Tadeu University, São Paulo, SP, Brazil. bruno.rodrigues@incor.usp.br
authors.forename: Bruno
authors.initials: B
authors.lastname: Rodrigues
authors.forename: Diego Mendrot Taboas
authors.initials: DM
authors.lastname: Figueroa
authors.forename: Jiao
authors.initials: J
authors.lastname: Fang
authors.forename: Kaleizu Teodoro
authors.initials: KT
authors.lastname: Rosa
authors.forename: Suzana
authors.initials: S
authors.lastname: Llesuy
authors.forename: Kátia
authors.initials: K
authors.lastname: De Angelis
authors.forename: Maria Cláudia
authors.initials: MC
authors.lastname: Irigoyen
mesh_terms: D000818:Animals; D002374:Catalase / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology*; D006943:Hyperglycemia / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin; D015996:Survival Rate; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D018487:Ventricular Dysfunction, Left / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D013311:Streptozocin; D002374:Catalase