Impact of myocardial infarction on cardiac autonomic function in diabetic rats

Autor(es)

Rodrigues, Bruno ^{[1, 2]} ; Mostarda, Cristiano T. ^[2] ; Jorge, Luciana ^[2] ; Barboza, Catarina A. ^[1] ; Grans, Camilla F. ^[1] ; De Angelis, Katia ^[3] ; Irigoyen, Maria Claudia ^[2]

Afiliação do(s) autor(es)

^[1] Univ Sao Judas Tadeu, Human Movement Lab, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Sch Med, Hypertens Unit, Heart Inst InCor, Sao Paulo - Brazil

^[3] Nove Julho Univ, Translat Physiol Lab, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF DIABETES AND ITS COMPLICATIONS; v. 27, n. 1, p. 16-22, JAN-FEB 2013.
• Citações Web of Science: 8

Resumo

Aims: We evaluated autonomic and hemodynamic parameters and maximal oxygen consumption (VO(2)max) as possible determinants of mortality in streptozotocin (STZ) diabetic rats after myocardial infarction (MI). Method: Male Wistar rats were divided into (n=8 of each): control sham (CS), diabetes sham (DS), MI (I), and diabetes +MI (DI). MI was induced 15 days after STZ induction. VO(2)max was measured at 3 (basal), 30, 60, and 91 days after MI. Hemodynamic and autonomic parameters were evaluated 92 days after MI. Results: MI area was similar in infarcted groups (similar to 44%). Mortality rate increased in the DI (70%) compared with I (53%) group. Cardiopulmonary baroreflex, sympathetic (48%) and vagal (33%) tonus, low frequency (LF) band (57%), and LF/high frequency (HF) band ratio (53%) were reduced in DI compared with I animals. Furthermore, cardiac output (CO), peripheral vascular resistance (PVR) impairment, and VO(2)max reductions were observed in the DI compared with the I group. Conclusions: Our data suggest that the CO and PVR changes as well as VO(2)max reduction were probably associated with additional cardiac autonomic control impairment, and, consequently, increased mortality rate in diabetic rats after a chronic myocardial infarction. (C) 2013 Elsevier Inc. All rights reserved. (AU)

• Processo FAPESP: 07/58942-0 - Da bancada à clínica: desenvolvimento de biomarcadores como preditores da resposta à terapêutica e lesão de órgãos-alvo na hipertensão arterial sistemática
• Beneficiário: Eduardo Moacyr Krieger
• Modalidade de apoio: Auxílio à Pesquisa - Temático