ArticleClinics (Sao Paulo, Brazil)2011
Short-term diabetes attenuates left ventricular dysfunction and mortality rates after myocardial infarction in rodents.
Article in Clinics (Sao Paulo, Brazil), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Mitochondria as a target of cardioprotection in models of preconditioning.Journal of bioenergetics and biomembranes · 2017Review
- Glucose and fatty acid metabolism in infarcted heart from streptozotocin-induced diabetic rats after 2 weeks of tissue remodeling.Cardiovascular diabetology · 2015Article
- Role of exercise training on autonomic changes and inflammatory profile induced by myocardial infarction.Mediators of inflammation · 2014Review
- Fasting hyperglycemia increases in-hospital mortality risk in nondiabetic female patients with acute myocardial infarction: a retrospective study.International journal of endocrinology · 2014Article
- Cardiovascular research in CLINICS.Clinics (Sao Paulo, Brazil) · 2013Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
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Abstract
objectivesTo investigate the effects of hyperglycemia on left ventricular dysfunction, morphometry, myocardial infarction area, hemodynamic parameters, oxidative stress profile, and mortality rate in rats that had undergone seven days of myocardial infarction.
introductionPrevious research has demonstrated that hyperglycemia may protect the heart against ischemic injury.
methodsMale Wistar rats were divided into four groups: control-sham, diabetes-sham, myocardial infarction, and diabetes + myocardial infarction. Myocardial infarction was induced 14 days after diabetes induction. Ventricular function and morphometry, as well as oxidative stress and hemodynamic parameters, were evaluated after seven days of myocardial infarction.
resultsThe myocardial infarction area, which was similar in the infarcted groups at the initial evaluation, was reduced in the diabetes + myocardial infarction animals (23 ± 3%) when compared with the myocardial infarction (42 ± 7%, p < 0.001) animals at the final evaluation. The ejection fraction (22%, p = 0.003), velocity of circumferential fiber shortening (30%, p = 0.001), and left ventricular isovolumetric relaxation time (26%, p = 0.002) were increased in the diabetes + myocardial infarction group compared with the myocardial infarction group. The diabetes-sham and diabetes + myocardial infarction groups displayed increased catalase concentrations compared to the control-sham and myocardial infarction groups (diabetes-sham: 32 ± 3; diabetes + myocardial infarction: 35 ± 0.7; control-sham: 12 ± 2; myocardial infarction: 16 ± 0.1 pmol min⁻¹ mg⁻¹ protein). The levels of thiobarbituric acid-reactive substances were reduced in the diabetes-sham rats compared to the control-sham rats. These positive adaptations were reflected in a reduced mortality rate in the diabetes + myocardial infarction animals (18.5%) compared with the myocardial infarction animals (40.7%, p = 0.001).
conclusionsThese data suggest that short-term hyperglycemia initiates compensatory mechanisms, as demonstrated by increased catalase levels, which culminate in improvements in the ventricular response, infarcted area, and mortality rate in diabetic rats exposed to ischemic injury.
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