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Updated: Apr 24, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Effect of metoprolol on myocardial apoptosis after coronary microembolization in rats
Qiang Su1, Lang Li1, Yang-Chun Liu1
1Department of Cardiology, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
Background:
Coronary microembolization (CME) is a serious complication following percutaneous coronary intervention (PCI) in patients with acute coronary syndromes. The use of metoprolol before PCI can significantly protect ischemic myocardium from myocardial damage, but the function of metoprolol in the treatment of CME is not entirely clear. This study was to explore the effect and significance of metoprolol on myocardial apoptosis and caspase-3 activation after CME in rats.
Methods:
Thirty rats were randomly divided into three groups including sham-operation (control group), CME plus saline (CME group), CME plus metoprolol (metoprolol group), 10 rats for each group. The CME group was induced by injecting 3 000 polyethylene microspheres (42 μm) into the left ventricle during a 10-second occlusion of the ascending aorta; the control group was injected with physiological saline instead of microembolization ball; the metoprolol or saline group was given three intravenous bolus injections before CME. Echocardiography, TUNEL staining, and Western blotting were used to evaluate cardiac function, proportion of apoptotic cells and activation of caspase-3 respectively at 6 hours after operation.
Results:
Echocardiographic parameters displayed that the metoprolol group improved cardiac function significantly compared with the CME group (P<0.05). The myocardial apoptotic rate of the CME group as well as the contents of activated caspase-3 increased significantly (P<0.05), both of which were ameliorated significantly by metoprolol treatment (P<0.05).
Conclusions:
This study demonstrates that metoprolol can protect the myocardium during CME in rats by inhibiting apoptosis and improving cardiac function. These results suggest that the inhibition of apoptosis can be a potential therapeutic strategy for the treatment of CME.
Insights
Metoprolol protects the heart from damage after coronary microembolization (CME) in rats. It reduces myocardial apoptosis and improves cardiac function, suggesting a potential therapeutic role for CME treatment.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Cellular Biology
Background:
- Coronary microembolization (CME) is a significant complication of percutaneous coronary intervention (PCI) in acute coronary syndromes.
- Metoprolol is known to protect ischemic myocardium, but its role in CME treatment remains unclear.
Purpose of the Study:
- To investigate the effects of metoprolol on myocardial apoptosis and caspase-3 activation following CME in a rat model.
- To assess the potential therapeutic significance of metoprolol in mitigating CME-induced cardiac damage.
Main Methods:
- Rats were divided into sham-operation, CME plus saline, and CME plus metoprolol groups.
- CME was induced using polyethylene microspheres; metoprolol or saline was administered intravenously prior to CME.
- Cardiac function, apoptotic cell proportion (TUNEL staining), and activated caspase-3 levels (Western blotting) were evaluated.
Main Results:
- Metoprolol treatment significantly improved cardiac function compared to the CME group.
- Myocardial apoptotic rate and activated caspase-3 levels were significantly elevated in the CME group.
- Metoprolol significantly ameliorated both myocardial apoptosis and caspase-3 activation.
Conclusions:
- Metoprolol demonstrates cardioprotective effects during CME in rats by inhibiting apoptosis and enhancing cardiac function.
- Inhibition of apoptosis emerges as a promising therapeutic strategy for managing CME.
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