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Updated: Jun 6, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
[The effects of nitric oxide on cardiac apoptosis and function during myocardial/reperfusion injury]
Ming-Zhong Ying1, Xiao-Ying Li, Xiao Chen
1Geriatric Department, Chinese PLA General Hospital, Beijing 100853, China.
Aim:
The observation of the relationship between the level of NO detected by ESR in the blood and the myocardial apoptosis and function caused by the recurrent, reversible myocardial ischemia/reperfusion injury.
Methods:
Fifteen New Zealand white rabbits were randomly divided into three groups (n = 5): (1) control group, (2) L-Arg group, (3) L-NNA group. The rabbits were anesthetized with intravenous pentobarbital. A suture ligature was passed around the left anterior descending coronary artery (LAD), so it could be snare occluded and reperfused. The LAD was occluded for 10 min three times, the first and second occlusions were followed by 10 min of reflow, after the third occlusion, the reperfusion was 120 min.
Results:
In all groups dp/dt(max) began to decrease at 5 min after the first ischemia. But compared with control group at 5 min after first reperfusion: in L-Arg group NO and apoptosis level were elevated but dp/dt(max) decreased significantly. In L-NNA group NO and apoptosis decreased significantly, dp/dt(max) improved significantly.
Conclusion:
The fact that the level of NO and apoptosis elevated suggested that they had taken part in the process of myocardial stunning.
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