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Updated: May 29, 2026
In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
5'- Adenosine monophosphate induced hypothermia reduces early stage myocardial ischemia/reperfusion injury in a mouse
Zhenyin Tao1, Zhaoyang Zhao, Cheng Chi Lee
1Department of Biochemistry and Molecular Biology, Medical School of The University of Texas Health Science Center at Houston Houston TX 77225, USA.
Abstract:
Early intervention using hypothermia treatment has been shown to reduce early inflammation, apoptosis and infarct size in animal models of cardiac ischemia/reperfusion. We have shown that 5'-adenosine monophosphate (5'-AMP) can induce a reversible deep hypothermia in mammals. We hypothesize that 5'-AMP-induced hypothermia (AIH) may reduce ischemic/reperfusion damage following myocardial infarct. C57BL/6J male mice were subjected to myocardial ischemia by ligating the left anterior descending coronary artery (LAD) followed by reperfusion. Compared to euthermic controls, mice given AIH treatment exhibited significant inhibition of neutrophil infiltration and a reduction in matrix metallopeptidase 9 (MMP-9) expressions in the infarcted myocardium. A decrease in terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive nuclei in the left ventricle myocardium were also observed. The overall infarct size of the heart was significantly smaller in AIH treated mice. Myocardial ischemia in mice given 5'-AMP without hypothermia had similar ischemia/reperfusion injuries as the euthermic control. Thus, the AIH cardio-protective effects were primarily hypothermia based.
Insights
5'-adenosine monophosphate-induced hypothermia (AIH) significantly reduces heart attack damage in mice by lowering inflammation and cell death. The protective effects are linked to hypothermia, not the drug alone.
Area of Science:
- Cardiology
- Cardiovascular Research
- Ischemia/Reperfusion Injury
Background:
- Hypothermia treatment is a known method for reducing inflammation, apoptosis, and infarct size in cardiac ischemia/reperfusion injury.
- 5 -adenosine monophosphate (5 -AMP) can induce reversible deep hypothermia in mammals.
Purpose of the Study:
- To investigate the potential cardioprotective effects of 5 -AMP-induced hypothermia (AIH) against myocardial infarction and ischemia/reperfusion damage.
- To determine if AIH reduces inflammation, apoptosis, and infarct size in a mouse model of myocardial infarction.
Main Methods:
- C57BL/6J male mice underwent myocardial ischemia via left anterior descending coronary artery ligation, followed by reperfusion.
- Mice were treated with AIH, and compared to euthermic controls.
- Assessed neutrophil infiltration, matrix metallopeptidase 9 (MMP-9) expression, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive nuclei.
Main Results:
- AIH treatment significantly inhibited neutrophil infiltration in the infarcted myocardium.
- Reduced expression of MMP-9 and decreased TUNEL-positive nuclei were observed in AIH-treated mice.
- AIH significantly reduced overall heart infarct size compared to controls. 5 -AMP without hypothermia did not show similar protective effects.
Conclusions:
- AIH demonstrates significant cardioprotective effects against ischemia/reperfusion injury, primarily mediated by hypothermia.
- The study confirms that hypothermia, induced by 5 -AMP, is the key factor in reducing myocardial damage.
- AIH represents a potential therapeutic strategy for managing myocardial infarction by mitigating reperfusion injury.
