title: Protective Effect of Antiapoptosis Potency of Prolonged Preservation by Desiccation Using High-Pressure Carbon Monoxide on Isolated Rabbit Hearts.
abstract: 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.
authors.affiliation: Southern Medical University, Guangzhou, China; Department of Cardiovascular Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
authors.forename: P Y
authors.initials: PY
authors.lastname: Zhou
authors.affiliation: Department of Cardiovascular Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
authors.forename: Z
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Department of Cardiovascular Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
authors.forename: Y L
authors.initials: YL
authors.lastname: Guo
authors.affiliation: Department of Cardiovascular Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
authors.forename: Z Z
authors.initials: ZZ
authors.lastname: Xiao
authors.affiliation: Department of Cardiovascular Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
authors.forename: P
authors.initials: P
authors.lastname: Zhu
authors.affiliation: Department of Cardiovascular Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
authors.forename: M J
authors.initials: MJ
authors.lastname: Mai
authors.affiliation: Department of Cardiovascular Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China. Electronic address: shaoyizheng@yahoo.com.
authors.forename: S Y
authors.initials: SY
authors.lastname: Zheng
mesh_terms: D000818:Animals; D017209:Apoptosis; D002248:Carbon Monoxide; D002314:Cardioplegic Solutions; D053148:Caspase 3 / Q000378:metabolism; D015925:Cryopreservation; D003890:Desiccation / Q000379:methods*; D006321:Heart; D016027:Heart Transplantation; D020287:In Situ Nick-End Labeling; D009926:Organ Preservation / Q000379:methods*; D011312:Pressure; D011817:Rabbits; D015427:Reperfusion Injury / Q000517:prevention & control
chemical_list: D002314:Cardioplegic Solutions; D002248:Carbon Monoxide; D053148:Caspase 3