Short-Term Fasting Reduces the Extent of Myocardial Infarction and Incidence of Reperfusion Arrhythmias in Rats
Short-Term Fasting Reduces the Extent of Myocardial Infarction and Incidence of Reperfusion Arrhythmias in Rats
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DOI：
10.33549/physiolres.932338
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发表时间：
2012-01-01
影响因子：
2.1
通讯作者：
Herget, J.
中科院分区：
文献类型：
--
作者：
Snorek, M.;Hodyc, D.;Herget, J.
研究了3天禁食对成年雄性Wistar大鼠心肌缺血耐受性的影响。麻醉开胸动物（戊巴比酮60 mg/kg， i.p）进行20 min左冠状动脉前降支闭塞，3 h再灌注测定梗死面积。在缺血和再灌注开始时（3分钟）监测室性心律失常。测定心肌β -羟基丁酸和乙酰乙酸浓度，评估线粒体氧化还原状态。与对照组（74.3 +/- 2.2%）相比，短期禁食限制了梗死面积（48.5 +/- 3.3%），与对照组（194.9 +/- 21.9）相比，减少了过早心室复合体的总数（12.5 +/- 5.8），以及早期再灌注时发生的室性心动过速持续时间（0.6 +/- 0.4秒vs. 18.8 +/- 2.5秒）。此外，与对照组（7.9 +/- 1.7）相比，禁食增加了β -羟丁酸浓度和β -羟丁酸/乙酰乙酸比值（87.8 +/- 27.0），反映了线粒体氧化还原状态的改变。综上所述，3天禁食可有效保护大鼠心脏免受急性I/R损伤的主要终点。需要进一步的研究来发现这些有益的影响是否与线粒体氧化还原状态的改变有关。
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.