title: Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents.
abstract: BACKGROUND
  Although clinical diabetes mellitus is obviously a high risk factor for myocardial infarction (MI), in experimental studies disagreement exists about the sensitivity to ischemic injury of an infarcted myocardium. Recently, our group demonstrated that diabetic animals presented better cardiac function recovery and cellular resistance to ischemic injury than nondiabetics. In the present study, we evaluated the chronic effects of MI on left ventricular (LV) and autonomic functions in streptozotocin (STZ) diabetic rats.
  
  
  METHODS
  Male Wistar rats were divided into 4 groups: control (C, n = 15), diabetes (D, n = 16), MI (I, n = 21), and diabetes + MI (DI, n = 30). MI was induced 15 days after diabetes (STZ) induction. Ninety days after MI, LV and autonomic functions were evaluated (8 animals each group). Left ventricular homogenates were analyzed by Western blotting to evaluate the expression of calcium handling proteins.
  
  
  RESULTS
  MI area was similar in infarcted groups (~43%). Ejection fraction and +dP/dt were reduced in I compared with DI. End-diastolic pressure was additionally increased in I compared with DI. Compared with DI, I had increased Na(+)-Ca(2+) exchange and phospholamban expression (164%) and decreased phosphorylated phospholamban at serine(16) (65%) and threonine(17) (70%) expression. Nevertheless, diabetic groups had greater autonomic dysfunction, observed by baroreflex sensitivity and pulse interval variability reductions. Consequently, the mortality rate was increased in DI compared with I, D, and C groups.
  
  
  CONCLUSIONS
  LV dysfunction in diabetic animals was attenuated after 90 days of myocardial infarction and was associated with a better profile of calcium handling proteins. However, this positive adaptation was not able to reduce the mortality rate of DI animals, suggesting that autonomic dysfunction is associated with increased mortality in this group. Therefore, it is possible that the better cardiac function has been transitory, and the autonomic dysfunction, more prominent in diabetic group, may lead, in the future, to the cardiovascular damage.
authors.affiliation: Human Movement Laboratory, São Judas Tadeu University, São Paulo, Brazil. bruno.rodrigues@incor.usp.br
authors.forename: Bruno
authors.initials: B
authors.lastname: Rodrigues
authors.forename: Kaleizu T
authors.initials: KT
authors.lastname: Rosa
authors.forename: Alessandra
authors.initials: A
authors.lastname: Medeiros
authors.forename: Beatriz D
authors.initials: BD
authors.lastname: Schaan
authors.forename: Patricia C
authors.initials: PC
authors.lastname: Brum
authors.forename: Kátia
authors.initials: K
authors.lastname: De Angelis
authors.forename: Maria Cláudia
authors.initials: MC
authors.lastname: Irigoyen
mesh_terms: D000818:Animals; D001342:Autonomic Nervous System Diseases / Q000503:physiopathology*; D048909:Diabetes Complications / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental; D006943:Hyperglycemia / Q000503:physiopathology*; D008297:Male; D009203:Myocardial Infarction / Q000150:complications* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D018487:Ventricular Dysfunction, Left / Q000378:metabolism / Q000503:physiopathology*