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Updated: Aug 22, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Apomorphine prevents myocardial ischemia/reperfusion-induced oxidative stress in the rat heart
Igor Khaliulin1, Aviva Schneider, Esther Houminer
1The Joseph Lunenfeld Cardiac Surgery Research Center, Hadassah--Hebrew University Medical Center, P.O. Box 12000, Jerusalem 91120, Israel.
Abstract:
This study examined the hypothesis that low-concentration apomorphine improves postischemic hemodynamic and mitochondrial function in the isolated rat heart model by attenuating oxidation of myocardial proteins. Control and apomorphine-treated hearts were subjected to 35 min of perfusion, 25 min of normothermic global ischemia, and 60 min of reperfusion. Apomorphine (2 microM) was introduced into the perfusate for 20 min starting from the onset of reperfusion. Apomorphine significantly (p <.05) improved postischemic hemodynamic function: work index of the heart (product of LVDP and heart rate) was twice as high in apomorphine-treated hearts compared to controls at the end of reperfusion (p <.01). After isolation of cardiac mitochondria, the respiratory control ratio (RCR) was calculated from the oxygen consumption rate of State 3 and State 4 respiration. Apomorphine significantly improved postischemic RCR (87% of preischemic value vs. 39% in control, p <.05). Using an immunoblot technique, carbonyl content of multiple unidentified myocardial proteins (mitochondrial and nonmitochondrial) was observed to be elevated after global ischemia and reperfusion. Apomorphine significantly attenuated the increased protein oxidation at the end of reperfusion. These results support the conclusion that apomorphine is capable of preventing ischemia/reperfusion-induced oxidative stress and thereby attenuating myocardial protein oxidation and preserving mitochondrial respiration function.
Insights
Low-concentration apomorphine enhances recovery of heart function after ischemia by reducing protein oxidation and preserving mitochondrial respiration. This study in isolated rat hearts demonstrates apomorphine
Area of Science:
- Cardiovascular Research
- Mitochondrial Biology
- Oxidative Stress
Background:
- Ischemia and reperfusion injury significantly impairs cardiac function.
- Oxidative stress and myocardial protein oxidation contribute to this damage.
- Mitochondrial dysfunction is a key consequence of ischemia-reperfusion.
Purpose of the Study:
- To investigate if low-concentration apomorphine protects isolated rat hearts from ischemia/reperfusion injury.
- To determine if apomorphine attenuates myocardial protein oxidation and preserves mitochondrial function.
Main Methods:
- Isolated rat hearts were subjected to global ischemia and reperfusion.
- Apomorphine (2 microM) was administered during reperfusion.
- Hemodynamic function (work index), mitochondrial respiration (respiratory control ratio), and protein oxidation (carbonyl content) were assessed.
Main Results:
- Apomorphine significantly improved postischemic hemodynamic function (work index doubled).
- Apomorphine preserved mitochondrial respiratory control ratio (87% vs. 39% of preischemic levels).
- Apomorphine attenuated ischemia/reperfusion-induced myocardial protein oxidation.
Conclusions:
- Low-concentration apomorphine effectively protects the heart against ischemia/reperfusion injury.
- Apomorphine's protective effects are mediated by reducing oxidative stress and preserving mitochondrial function.
- Apomorphine demonstrates potential as a therapeutic agent for cardiac ischemia.
