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Updated: Aug 10, 2026
LAD-Ligation: A Murine Model of Myocardial Infarction
Published on: October 14, 2009
dl-3-Hydroxybutyrate administration prevents myocardial damage after coronary occlusion in rat hearts
Zhitian Zou1, Shiro Sasaguri, Katare Gopalrao Rajesh
1Department of Surgery II, Kochi Medical School, Nankoku, Kochi 783-8505, Japan.
Insights
High concentrations of dl-3-hydroxybutyrate (DL-3-HB) significantly reduce heart damage and apoptosis after prolonged fasting and ischemia-reperfusion. This ketone body may protect the heart by providing an essential energy substrate.
Area of Science:
- Cardiovascular Science
- Metabolic Research
- Cellular Biology
Background:
- Prolonged fasting can alter myocardial energy metabolism.
- Ischemia-reperfusion injury is a significant cause of heart damage.
- Ketone bodies, like DL-3-HB, are alternative energy substrates.
Purpose of the Study:
- To investigate the cardioprotective role of high dl-3-hydroxybutyrate (DL-3-HB) concentrations in fasted rats.
- To determine the effects of DL-3-HB on infarct size and apoptosis following ischemia-reperfusion.
- To assess the impact of DL-3-HB on myocardial ATP levels during fasting and ischemia-reperfusion.
Main Methods:
- Wistar rats were divided into fed and fasted groups, with and without DL-3-HB administration.
- Myocardial ischemia was induced by left coronary artery occlusion (30 min) followed by reperfusion (120 min).
- Infarct size was quantified using triphenyltetrazolium chloride staining, and apoptosis was assessed via single-stranded DNA staining.
Main Results:
- DL-3-HB administration significantly reduced infarct size in fasted rats (26% vs. 70-75% in other groups).
- Apoptosis was markedly decreased in the subendocardial region of the fasting + DL-3-HB group (9% vs. 34-39% in others).
- ATP levels were significantly higher in the fasting + DL-3-HB group post-ischemia-reperfusion.
Conclusions:
- High concentrations of DL-3-HB effectively reduce myocardial infarction size and apoptosis induced by ischemia-reperfusion in fasted rats.
- DL-3-HB may exert its cardioprotective effects by serving as an energy substrate for the myocardium.
- These findings suggest a potential therapeutic role for DL-3-HB in managing cardiac injury associated with fasting or metabolic stress.
Abstract:
To investigate the role of high concentrations of dl-3-hydroxybutyrate (DL-3-HB) in preventing heart damage after prolonged fasting, infarct size and the incidence of apoptosis caused by ischemia-reperfusion were determined in four groups of Wistar rats. Fed rats (+/-DL-3-HB group) and fasted rats (+/-DL-3-HB group) were subjected to 30 min of left coronary artery occlusion and 120 min of reperfusion. DL-3-HB was administered intravenously 60 min before the coronary artery occlusion. Infarct size, defined by triphenylyetrazolium chloride (TTC) staining, was reduced from 72 +/- 3% (fed group), 75 +/- 5% (fed + DL-3-HB group), and 70 +/- 5% (fasting group), respectively, to 26 +/- 4% (P < 0.01 vs. fasting + DL-3-HB group). Apoptosis, as defined by single-stranded DNA staining, was significantly reduced in the subendocardial region in the fasting + DL-3-HB group (9 +/- 2%) compared with the other groups (39 +/- 6% in the fed group, 37 +/- 5% in the fed + DL-3-HB group, and 34 +/- 3% in the fasting group; P < 0.01). In addition, levels of ATP in the fasting + DL-3-HB group were significantly higher compared with other groups after 30 min of ischemia and 120 min of reperfusion (P < 0.01). In conclusion, the present study demonstrates that high concentrations of DL-3-HB reduces myocardial infarction size and apoptosis induced by ischemia-reperfusion, possibly by providing increased energy substrate to the fasted rat myocardium.
