Abstract
BackgroundPrevious 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).MethodsDiabetes 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).ResultsThe 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).ConclusionsThese 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.
Highlights
It is well established that cardiovascular autonomic neuropathy is a major complication of diabetes
DBP was decreased after diabetes and myocardial infarction (D: 82 ± 2; myocardial infarcted (MI): 82 ± 2; diabetic myocardial infarcted (DMI): 89 ± 3 mmHg) when compared to controls (96 ± 2 mmHg)
MBP was reduced in diabetic group (D: 92 ± 2 mmHg) when compared to control group (C: 105 ± 2 mmHg), and was not altered after myocardial infarction (MI: ± 3 and DMI: ± 3 mmHg)
Summary
It is well established that cardiovascular autonomic neuropathy is a major complication of diabetes. It is a common manifestation in diabetics and contributes to the overall clinical pathology [1,2]. Our group has previously demonstrated that left ventricular dysfunction in chronic diabetic animals was attenuated after 90 days of myocardial infarction. This finding was associated with better profile of calcium handling proteins in left ventricle of diabetic infarcted rats [13]. 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)
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