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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.)

Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats

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Author(s):
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Malfitano, Christiane [1] ; Barboza, Catarina Andrade [2] ; Mostarda, Cristiano [3, 4] ; da Palma, Renata Kelly [1] ; dos Santos, Camila Paixao [1] ; Rodrigues, Bruno [2] ; Ferreira Freitas, Sarah Cristina [1] ; Bello-Klein, Adriane [1, 5] ; Llesuy, Susana [1, 6] ; Irigoyen, Maria-Claudia [3] ; De Angelis, Katia [1]
Total Authors: 11
Affiliation:
[1] Univ Nove de Julho UNINOVE, Translat Physiol Lab, BR-01504001 Sao Paulo - Brazil
[2] Univ Sao Judas Tadeu UST, Human Movement Lab, Sao Paulo - Brazil
[3] Univ Sao Paulo, Sch Med, Heart Inst InCor, Hypertens Unit, Sao Paulo - Brazil
[4] Univ Fed Maranhao UFMA, Sao Luis, MA - Brazil
[5] Univ Fed Rio Grande do Sul, Lab Fisiol Cardiovasc & Especies Ativas Oxigenio, Porto Alegre, RS - Brazil
[6] Univ Buenos Aires, Fac Farm & Bioquim, Catedra Quim Gen & Inorgan, RA-1113 Buenos Aires, DF - Argentina
Total Affiliations: 6
Document type: Journal article
Source: CARDIOVASCULAR DIABETOLOGY; v. 13, OCT 10 2014.
Web of Science Citations: 10
Abstract

Background: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. The aim of the present study was to investigate the association between hyperglycemia and myocardial infarction on cardiovascular autonomic modulation and cardiac oxidative stress profile in rats. Male Wistar rats were divided into: control (C), diabetic (D), myocardial infarcted (MI) and diabetic infarcted rats (DMI). Methods: Diabetes was induced by streptozotocin (STZ, 50 mg/Kg) at the beginning of the protocol and MI was induced by left coronary occlusion 15 days after STZ. Thirty days after streptozocin-induced diabetes, cardiovascular autonomic modulation was evaluated by spectral analysis, and oxidative stress profile was determined by antioxidant enzyme activities and superoxide anion, together with protein carbonylation and redox balance of glutathione (GSH/GSSG). Results: The diabetic and infarcted groups showed decreased heart rate variability and vagal modulation (p < 0.05); however, sympathetic modulation decreased only in diabetic groups (p < 0.05). Sympatho/vagal balance and vascular sympathetic modulation were increased only in the MI group (p < 0.05). Diabetes promoted an increase in catalase concentration (p < 0.05). Glutathione peroxidase activity was increased only in DMI when compared to the other groups (p < 0.05). Superoxide anion and protein carbonylation were increased only in MI group (p < 0.05). Cardiac redox balance, as evaluated by GSH/GSSG, was lower in the MI group (p < 0.05). Conclusions: These data suggest that hyperglycemia promotes compensatory mechanisms that may offer protection against ischemia, as demonstrated by increased antioxidants, decreased pro-oxidants and protein damage, possibly related to the improvements in both redox balance and sympathetic modulation to the heart. (AU)

FAPESP's process: 12/20141-5 - Effects of aerobic,resistance or combined exercise training in experimental models of cardiometabolic disorders associated with ovarian hormone deprivation
Grantee:Kátia de Angelis Lobo D Avila
Support Opportunities: Regular Research Grants
FAPESP's process: 14/18685-2 - Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats
Grantee:Christiane Malfitano
Support Opportunities: Regular Research Grants - Publications - Scientific article