Background: Storage of hearts in ice for transportation is thought to cause post-transplantation graft dysfunction secondary to freeze injury. We studied the myocardial damage and resulting function in hearts stored at 0 °C, 4 °C and 8 °C for 4 hours.
Methods: Rat hearts were procured under general anesthesia and immediately stored in University of Wisconsin solution at 0 °C, 4 °C and 8 °C for 4 hours (n = 6-8/group). Hearts were then re-perfused on a Langendorff apparatus for 90 minutes using oxygenated Kreb-Henseleit buffer (37 °C). Functional parameters were recorded via a balloon tip catheter in the left ventricle. Following reperfusion hearts were collected for infarct size quantification using triphenyltetrazolium chloride staining. A separate group of hearts (n = 2-3) were similarly stored then studied for ultrastructural and biochemical changes.
Results: There were no signs of freeze injury in hearts stored at 0 °C by histologic or biochemical analysis. There was no significant difference in infarct size between hearts stored at 0 °C and 4 °C. Cardiac troponin I level, and left ventricle developed pressure in hearts stored at 0 °C, 4 °C, and 8 °C were comparable (all P > .05).
Conclusion: Hearts stored at 0 °C for 4 hours showed no signs of freeze injury and had similar functional parameters compared to hearts stored at 4 °C or 8 °C.
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