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目的：探讨ＡＴＰＭｇＣｌ２心停搏液对发育未成熟心肌的保护作用。方法：采用离体心作功模型，观察局部单低温（１０～１５℃）、改良Ｔｈｏｍａｓ液和ＡＴＰＭｇＣｌ２心停搏液加低温单剂灌注对未成熟兔心肌缺血１２０分钟、再灌注６０分钟后能量代谢变化的影响。结果：缺血再灌注后，ＡＴＰＭｇＣｌ２心停搏液灌注组游离腺苷酸总量（ＡＮＰ）、三磷酸腺苷（ＡＴＰ）、二磷酸腺苷（ＡＤＰ）含量均优于其它２组；而一磷酸腺苷（ＡＭＰ）、心肌线粒体丙二醛（ＭＤＡ）及冠状动脉流出液中肌酸磷酸激酶（ＣＰＫ）、乳酸脱氢酶（ＬＤＨ）和谷草转氨酶（ＧＯＴ）含量均低于另２组。结论：ＡＴＰＭｇＣｌ２心停搏液具有改善未成熟兔心肌缺血再灌注后能量代谢的作用。
Objective: To investigate the protective effect of ATPMgCl2 cardioplegia on immature myocardium. Methods: The isolated heart function model was used to observe the effects of local single hypothermia (10 ~ 15 ℃), modified Thomas liquid and ATPMgCl2 cardioplegia plus single-dose hypothermia on immature rabbit myocardial ischemia for 120 minutes and 60 minutes after reperfusion The impact of changes in energy metabolism. Results: After ischemia-reperfusion, ATPMgCl2 cardioplegia perfusion group, free adenosine acid (ANP), adenosine triphosphate (ATP), adenosine diphosphate (ADP) content were better than the other two groups; and adenosine monophosphate (AMP), malondialdehyde (MDA) in myocardial mitochondria and CPK, lactate dehydrogenase (LDH) and aspartate aminotransferase (GOT) in coronary effluent were lower than those in the other two groups. Conclusion: ATPMgCl2 cardioplegia can improve the energy metabolism of immature rabbit after myocardial ischemia / reperfusion.