Cardiac surgery with crystalloid cardioplegia: Improved functional recovery due to molecular adaptations in adult rat hearts

Background: The effect of aging on functional recovery after a period of crystalloid cardioplegic arrest is still a matter of debate. We hypothesized that age-dependent differences in the polyamine metabolism may contribute to such differences. Methods: Hearts from juvenile and adult Wistar rats were placed in a perfused beating heart model and given Bretschneider's cardioplegia for an ischemia period of 60 min. During reperfusion, recovery of contractile function and coronary blood flow were measured for 90 min. In addition, adult hearts received putrescine to bypass polyamine metabolism during the 1st min of reperfusion. In comparison, the effect of putrescine was analyzed from hearts reperfused after 45-min flow arrest for 90 min. The rate-limiting enzyme of the polyamine metabolism, ornithine decarboxylase (ODC), the proapoptotic enzyme bax, and the relation between SR-calcium-ATPase (SERCA2a) and a natrium-calcium-exchanger enzyme were determined on mRNA-level through real-time polymerase chain reaction. Results: Adult hearts had lower basal performance and lower SERCA mRNA expression compared to juvenile hearts. However, after a 60-min aortic clamping period, recovery of left ventricular developed pressure (105.6 ± 39.7% of baseline) in the adult group was better than in the young group (61.3 ± 34.1% of baseline). ODC mRNA was significantly (P = 0.04228) lower in adult hearts (0.60 ± 0.09-fold vs. juvenile rats). Similar, bax mRNA was significantly (P = 0.01662) lower in adult hearts (0.22 ± 0.03-fold vs. juvenile rats). Addition of putrescine to adult hearts during reperfusion attenuated a better outcome of these hearts suggesting a detrimental effect of polyamine metabolism after cardioplegic arrest. In contrast, putrescine improved recovery in postischemic hearts without exposure to cardioplegic solution. Conclusion: Adult rat hearts tolerate cardioplegia-mitigated ischemia better than juvenile hearts because they express less ODC during resubstitution of normal calcium levels