Key result
Diabetic hyperglycemia attenuated sympathetic dysfunction after myocardial infarction in rats, significantly reducing the sympathovagal balance (LF/HF 0.14 vs 0.40) and improving the oxidative stress profile.
Why the study?
Does diabetic hyperglycemia attenuate sympathetic dysfunction and oxidative stress after myocardial infarction in rats?
Population
Male Wistar rats (2-3 months old, 250-270 g), n=32
Comparison
Streptozotocin-induced diabetes followed 15 days… vs Control rats, diabetic rats without infarction…
Design
Preclinical, The rats were randomly assigned to 4 groups
Follow-up
30 days
Authors
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Hypothesis-generating for autonomic protection by hyperglycemia post-MI in rats; should not change human diabetes management.
Does diabetic hyperglycemia attenuate sympathetic dysfunction and oxidative stress after myocardial infarction in rats?
Absolute Event Rate: 0.14% vs 0.4%
p-value: p=<0.05
Short-term diabetic hyperglycemia in rats promotes compensatory mechanisms that attenuate sympathetic dysfunction and oxidative stress following myocardial infarction.
Malfitano et al. (2014) studied Myocardial infarction and diabetes (n=32). Diabetic hyperglycemia (Streptozotocin-induced) vs. Normoglycemic myocardial infarction (citrate buffer) was evaluated on Sympathovagal balance (LF/HF) (p=<0.05). Diabetic hyperglycemia attenuated sympathetic dysfunction after myocardial infarction in rats, significantly reducing the sympathovagal balance (LF/HF 0.14 vs 0.40) and improving the oxidative stress profile.
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