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Updated: Aug 14, 2026

Model of Ischemia and Reperfusion Injury in Rabbits
Published on: November 3, 2023
Absence of apparent cardioprotection following ischemic preconditioning in immature rabbit hearts
1Department of Anaesthesiology, Peking Union Medical College Hospital, CAMS & PUMC, Beijing, PR China.
Background:
The cardioprotective effects of ischemic preconditioning (IPC) have been demonstrated in adult hearts of all species so far studied.
Aims:
To investigate whether IPC could protect immature rabbit hearts against ischemia-reperfusion injury in an isolated Langendorff-mode perfusion model.
Methods:
Hearts from 18 rabbits aged 14-21 days were randomly divided into two groups (an IPC group and a control group). After isolated Langendorff-mode perfused hearts were equilibrated the IPC stimulus in the IPC group was 5 min global ischemia followed by 10 min reperfusion. Hearts in both groups were then made globally ischemic for 30 min (no perfusion), followed by 40 min reperfusion. Coronary flow (CF), heart rate (HR), left ventricular developed pressure (LVDP), and +/-dp/dt(max) were monitored at equilibration (baseline value) and then 5, 10, 20, 30 and 40 min after reperfusion. The values obtained after reperfusion were expressed as a percentage of their baseline value. Arrhythmia severity, myocardial enzymes in the coronary effluent, and myocardial energy metabolism were also determined.
Results:
There were no statistical differences in postreperfusion CF, HR, LVDP and +/-dp/dt(max) between the two groups. Arrhythmia scores were also comparable between the two groups. The myocardial-specific isoenzyme of creatine kinase (CK-MB) leakage in the IPC group was increased, but not significantly different from that in the control group. At the end of reperfusion, the adenosine triphosphate (ATP) level in the myocardium in the IPC group was significantly lower than the level in the control group.
Conclusions:
This model of IPC was not able to protect juvenile rabbit hearts from ischemia-reperfusion injury. This study suggests that signal transduction pathways involved in triggering cardioprotective mechanisms may not be fully developed, or are not able to be invoked by the present model in juvenile rabbit.

