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Updated: Apr 4, 2026
Model of Ischemia and Reperfusion Injury in Rabbits
Published on: November 3, 2023
Protective effects of morphine preconditioning in delayed phase on myocardial ischemia-reperfusion injury in rabbits
1Department of Anesthesiology, the Second Xiangya Hospital, Central South University, Changsha, China.
Abstract:
The aim of this study was to investigate the protective mechanisms of delayed-phase morphine preconditioning on myocardial ischemia-reperfusion injury. Thirty healthy male New Zealand white rabbits were randomly divided into three groups: a sham operation group (C), ischemia-reperfusion group (I/R), and delayed-phase morphine preconditioning group (M) (N = 10/group). Rabbits in the C group received thoracotomy for 160 min. Rabbits in the I/R group received left artery blockage for 40 min and reperfusion for 120 min. Rabbits in the M group received 1.0 mg/kg intravenous morphine 24 h prior to the identical treatment as the rabbits in the I/R group. In each group, the interleukin (IL)-10 and tumor necrosis factor (TNF)-α levels were detected at five time points: 20 min before the left coronary artery blockage (T1), 20 and 40 min after the left coronary artery blockage (T2 and T3, respectively), and 1 and 2 h after the myocardial reperfusion (T4 and T5, respectively). After reperfusion, the infarction size was measured with Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) staining. Compared with the C group, serum IL-10 and TNF-α concentrations increased in the I/R and M groups; the difference was significant (P < 0.05). When compared with the I/R group, the IL-10 concentrations in the M group were significantly increased (P < 0.05), but the infarction size and TNF-α concentrations were significantly decreased (P < 0.05). These results suggested that delayed-phase morphine preconditioning might achieve myocardial protection through the regulation and balance of inflammatory cytokines.
Insights
Delayed-phase morphine preconditioning protects the heart from injury by modulating inflammatory cytokines. This study shows morphine preconditioning increases beneficial interleukin-10 and decreases harmful tumor necrosis factor-alpha, reducing heart damage.
Area of Science:
- Cardiology
- Pharmacology
- Immunology
Background:
- Myocardial ischemia-reperfusion injury (I/R) is a significant clinical problem.
- Inflammatory responses, involving cytokines like IL-10 and TNF-α, play a critical role in I/R injury.
- Morphine preconditioning is a potential therapeutic strategy, but its delayed-phase protective mechanisms require further investigation.
Purpose of the Study:
- To investigate the protective effects of delayed-phase morphine preconditioning on myocardial ischemia-reperfusion injury.
- To elucidate the role of inflammatory cytokines, specifically interleukin-10 (IL-10) and tumor necrosis factor-alpha (TNF-α), in morphine-mediated cardioprotection.
Main Methods:
- A rabbit model of myocardial ischemia-reperfusion was established.
- Rabbits received either sham operation, I/R, or delayed-phase morphine preconditioning (1.0 mg/kg IV morphine 24h prior to I/R).
- Serum IL-10 and TNF-α levels were measured at multiple time points, and myocardial infarction size was assessed using Evans blue and TTC staining.
Main Results:
- Both I/R and morphine preconditioning groups showed increased IL-10 and TNF-α compared to the sham group.
- Compared to the I/R group, morphine preconditioning significantly increased IL-10 levels (P < 0.05).
- Morphine preconditioning significantly decreased myocardial infarction size and TNF-α levels compared to the I/R group (P < 0.05).
Conclusions:
- Delayed-phase morphine preconditioning confers significant cardioprotection against ischemia-reperfusion injury.
- This protection is associated with an enhanced anti-inflammatory response, characterized by increased IL-10 and decreased TNF-α.
- Morphine preconditioning may represent a viable therapeutic approach for mitigating myocardial damage by balancing inflammatory cytokines.
