Short-Term Fasting Reduces the Extent of Myocardial Infarction and Incidence of Reperfusion Arrhythmias in Rats
| Autor: | František Kolář, J Durisova, V Sedivý, Jiri Wilhelm, Jan Herget, Michal Šnorek, Jan Neckář, Daniel Hodyc, A. Skoumalova |
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| Rok vydání: | 2012 |
| Předmět: |
Male
Tachycardia medicine.medical_specialty Physiology Myocardial Infarction Ischemia Myocardial Reperfusion Injury Anterior Descending Coronary Artery Ventricular tachycardia Acetoacetates Internal medicine Ketogenesis Occlusion medicine Animals Myocardial infarction Rats Wistar 3-Hydroxybutyric Acid business.industry Incidence (epidemiology) Arrhythmias Cardiac General Medicine medicine.disease Mitochondria Rats Tachycardia Ventricular Cardiology medicine.symptom business Oxidation-Reduction |
| Zdroj: | Scopus-Elsevier Publons |
| ISSN: | 1802-9973 0862-8408 |
| Popis: | The effect of three-day fasting on cardiac ischemic tolerance was investigated in adult male Wistar rats. Anesthetized open-chest animals (pentobarbitone 60 mg/kg, i.p.) were subjected to 20-min left anterior descending coronary artery occlusion and 3-h reperfusion for infarct size determination. Ventricular arrhythmias were monitored during ischemia and at the beginning (3 min) of reperfusion. Myocardial concentrations of beta-hydroxybutyrate and acetoacetate were measured to assess mitochondrial redox state. Short-term fasting limited the infarct size (48.5±3.3 % of the area at risk) compared to controls (74.3±2.2 %) and reduced the total number of premature ventricular complexes (12.5±5.8) compared to controls (194.9±21.9) as well as the duration of ventricular tachycardia (0.6±0.4 s vs. 18.8±2.5 s) occurring at early reperfusion. Additionally, fasting increased the concentration of beta-hydroxybutyrate and beta-hydroxybutyrate/acetoacetate ratio (87.8±27.0) compared to controls (7.9±1.7), reflecting altered mitochondrial redox state. It is concluded that three-day fasting effectively protected rat hearts against major endpoints of acute I/R injury. Further studies are needed to find out whether these beneficial effects can be linked to altered mitochondrial redox state resulting from increased ketogenesis. |
| Databáze: | OpenAIRE |
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