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Induction and Assessment of Ischemia-reperfusion Injury in Langendorff-perfused Rat Hearts
Published on: July 27, 2015
Interaction between pre- and postconditioning in the in vivo rat heart
Olivier C Manintveld1, Maaike te Lintel Hekkert, Nathalie T van der Ploeg
1Experimental Cardiology, Thoraxcenter, Cardiovascular Research School COEUR, Erasmus MC, University Medical Center Rotterdam, 3000 CA Rotterdam, The Netherlands.
Experimental Biology and Medicine (Maywood, N.J.)
|August 7, 2009
Summary
Ischemic postconditioning does not offer additional heart protection in preconditioned hearts, regardless of the preconditioning method or tolerance. This lack of added benefit may stem from both processes relying on nitric oxide synthase.
Area of Science:
- Cardiovascular Physiology
- Myocardial Ischemia Research
Background:
- Pre-infarct angina can precondition the heart, potentially affecting the efficacy of interventions like postconditioning.
- Understanding the interplay between preconditioning and postconditioning is crucial for optimizing cardioprotective strategies.
Purpose of the Study:
- To investigate if ischemic postconditioning provides additional cardioprotection in hearts already preconditioned by various methods.
- To determine the role of nitric oxide synthase in the interaction between preconditioning and postconditioning.
Main Methods:
- Anesthetized rats underwent 60-minute coronary artery occlusions (CAO).
- Hearts were either not preconditioned, preconditioned with single (1IPC15) or triple (3IPC3) brief CAOs, or pharmacologically preconditioned with adenosine.
- The effect of postconditioning was assessed in these groups, including those tolerant to 1IPC15, with and without nitric oxide synthase inhibition.
Main Results:
- Postconditioning limited infarct size in control hearts but offered no additional protection in preconditioned hearts.
- Nitric oxide synthase inhibition abolished cardioprotection from postconditioning, preconditioning stimuli, and their combination.
- Postconditioning failed to protect adenosine-preconditioned or tolerance-developed hearts.
- Postconditioning paradoxically increased infarct size after 30-min CAO, an effect abolished by preconditioning stimuli.
Conclusions:
- Postconditioning does not provide additional cardioprotection in preconditioned hearts, irrespective of the preconditioning stimulus or tolerance.
- The lack of additional benefit is likely due to both preconditioning and postconditioning being mediated via nitric oxide synthase.
- The interaction between preconditioning and postconditioning is highly dependent on the duration of ischemia but not the preconditioning stimulus.
