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Postconditioning the isolated working rat heart
Derick van Vuuren1, Amanda Genis, Sonia Genade
1Department of Biomedical Sciences, Division of Medical Physiology, Faculty of Health Sciences, University of Stellenbosch, P.O. Box 19063, Tygerberg, 7505, Republic of South Africa.
Insights
Postconditioning (postC) protects hearts from reperfusion injury. This study developed a cardioprotective postC protocol in a working heart model, showing infarct sparing effects sensitive to temperature.
Area of Science:
- Cardiovascular Physiology
- Ischemia-Reperfusion Injury
- Cardioprotection
Background:
- Postconditioning (postC) is a cardioprotective strategy against reperfusion injury.
- Its infarct-sparing effect in isolated working heart models remains unreported.
- Developing an effective postC protocol for this model is crucial.
Purpose of the Study:
- To develop a cardioprotective postconditioning protocol.
- To investigate the infarct-sparing effect of postC in an isolated working heart model.
- To assess the influence of temperature on postC efficacy.
Main Methods:
- Rat hearts perfused retrogradely (Langendorff) or in working mode.
- Global or regional ischemia followed by reperfusion.
- Postconditioning applied via brief ischemia/reperfusion cycles.
- Infarct size measured; temperature varied (36.5°C vs. 37°C).
Main Results:
- Postconditioning demonstrated an infarct-sparing effect at 37°C in both Langendorff and working heart models.
- Significant infarct reduction (p<0.0001 in Langendorff, p<0.001 in working).
- Functional preservation was observed only in the Langendorff group, not the working heart group.
Conclusions:
- An infarct-sparing effect of postconditioning was achieved in the working heart model.
- This effect was highly sensitive to temperature fluctuations.
- Functional preservation was not associated with infarct sparing in the working heart model.
Purpose:
Despite the attention focussed on postconditioning (postC; brief cycles of reperfusion/ischaemia at the onset of reperfusion, conferring cardioprotection against reperfusion injury), an infarct sparing effect for postC in the isolated working heart model has not been reported. The purpose of this study was to develop a cardioprotective postC protocol in this model.
Methods:
Hearts from male Wistar rats (210-350 g) were perfused either retrogradely (Langendorff) or in the working mode. For functional studies 30 or 35 min global ischaemia (GI) and 20 or 25 min GI were applied in the Langendorff and working heart models respectively. Infarct size was measured after 35 min regional ischaemia (RI) in both models. In the latter studies hearts were subdivided into low (36.5 degrees C) and high (37 degrees C) temperature groups (during both ischaemia and initial reperfusion). In all groups hearts were either freely reperfused (nonPostC) or postconditioned (postC) by 6x10 s ischaemia/reperfusion cycles.
Results:
In both perfusion modes postC only elicited an infarct sparing effect after a slight elevation in temperature to 37 degrees C (Langendorff: L-nonPostC=47.99+/-3.31% vs. L-postC=27.81+/-2.49%, p<0.0001; and work=W-nonPostC: 35.81+/-3.67% vs. W-postC=17.74+/-2.72%, p<0.001). However, only in the Langendorff group could postC conserve post-ischaemic function, while no significant recoveries were seen in the working hearts.
Conclusion:
We demonstrated an infarct sparing effect for postC in the working heart model, which unlike the Langendorff model, was not associated with functional preservation. The infarct sparing effect of postC in both models was however extremely sensitive to even slight fluctuations in temperature.
