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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents

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Author(s):
Rodrigues, Bruno [1, 2] ; Rosa, Kaleizu T. [1] ; Medeiros, Alessandra [3] ; Schaan, Beatriz D. [4] ; Brum, Patricia C. [5] ; De Angelis, Katia [6] ; Irigoyen, Maria Claudia [1]
Total Authors: 7
Affiliation:
[1] Univ Sao Paulo, Sch Med, Heart Inst InCor, Hypertens Unit, Sao Paulo - Brazil
[2] Univ Sao Judas Tadeu, Human Movement Lab, Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Biosci, Santos, SP - Brazil
[4] Univ Fed Rio Grande do Sul, Clin Hosp Porto Alegre, Div Endocrine, Porto Alegre, RS - Brazil
[5] Univ Sao Paulo, Sch Phys Educ & Sports, Sao Paulo - Brazil
[6] Nove de Julho Univ, Sao Paulo - Brazil
Total Affiliations: 6
Document type: Journal article
Source: CARDIOVASCULAR DIABETOLOGY; v. 10, APR 6 2011.
Web of Science Citations: 26
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 (similar to 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. (AU)

FAPESP's process: 01/00009-0 - An integrated approach for the dissection of primary hypertension: molecular and functional characterization of the cardiovascular system
Grantee:Eduardo Moacyr Krieger
Support Opportunities: Research Projects - Thematic Grants