Heart transplantation has been widely accepted as a therapy for end-stage heart failure. Mitigation of ischemia-reperfusion injury by inhibiting the apoptotic process plays an important role in organ transplantation. Desiccation using high-pressure carbon monoxide (CO) is a new method of preserving donor hearts; however, its mechanism of antiapoptosis remains unclear. This study was intended to elucidate the efficacy and mechanism of preservation by desiccation for 18 hours using high-pressure CO on myocardial apoptosis. Rabbit heterotopic abdominal cardiac transplantation models were established. New Zealand rabbits were divided randomly into 3 groups: naive group (n = 16), HTK group (n = 16), and desiccation using high-pressure CO group (n = 16). The donor hearts of the naive group were transplanted immediately after being extracted. In the HTK group, the donor hearts were extracted and steeped in 4°C HTK cardioplegic solution for 18 hours and then transplanted; in the desiccation using high-pressure CO group, the donor hearts were extracted and exposed to a gas mixture (Po2 = 3200 hPa, Pco = 800 hPa) in the chamber before being preserved in a refrigerator at 4°C for 18 hours and then transplanted. Apoptotic cardiomyocytes were detected using TUNEL technique and histopathology was performed by hematoxylin-eosin staining. The expression of the ratio of Bcl-2/Bax and caspase-3 proteins was detected using the Western blot method. These findings suggest that compared with traditional HTK preservation, preservation by desiccation using high-pressure CO could alleviate rabbits' myocardial histopathology and apoptosis induced by ischemia-reperfusion injury through adjusting the ratio of Bcl-2/Bax protein expression, thus resulting in the reduction of expression of caspase-3.
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