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. 2014 Oct 10:13:131.
doi: 10.1186/s12933-014-0131-x.

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

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

Christiane Malfitano et al. Cardiovasc Diabetol. .

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.

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Figures

Figure 1
Figure 1
Oxidative stress profile of left ventricle homogenates in control (C), diabetes (D), myocardial infarction (MI), and diabetes + myocardial infarction (DMI) rats (n = 8 for each group). A: Lipid peroxidation indicated by thiobarbituric acid-reactive substances (TBARS). B: protein carbonylation. *p < 0.05 vs. C; p < 0.05 vs. MI.
Figure 2
Figure 2
Oxidative stress profile of left ventricle homogenates in control (C), diabetes (D), myocardial infarction (MI), and diabetes + myocardial infarction (DMI) rats (n = 8 for each group). A: superoxide anion. B: catalase activity. C: superoxide dismutase activity. D: glutathione peroxidase activity. *p < 0.05 vs. C; p < 0.05 vs. MI; p < 0.05 vs. D.
Figure 3
Figure 3
Oxidized (GSH) and reduced glutathione (GSSG) ratio in left ventricle tissue in control (C), diabetes (D), myocardial infarction (MI), and diabetes + myocardial infarction (DMI) rats (n = 8 for each group). p < 0.05 vs. MI.
Figure 4
Figure 4
Pearson correlation analysis involving animals of all groups (C; D; MI and DMI). A: Cardiac sympathetic modulation (LF band of PI) and catalase. B: Cardiac sympathetic modulation (LF band of PI) and superoxide anion. C: Vascular sympathetic modulation (LF band of SAP) and GSH/GSSG ratio.

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