Julia P L, Buckberg G D, Acar C, Partington M T, Sherman M P
Department of Surgery, University of California, Los Angeles School of Medicine 90024-1741.
J Thorac Cardiovasc Surg. 1991 Feb;101(2):303-13.
Postischemic damage is caused partially by oxygen free radical-mediated injury. This study will show that (1) crystalloid cardioplegia with room air oxygen is deleterious because it is devoid of free radical scavengers and (2) blood cardioplegia limits damage because it contains endogenous free radical scavengers in red blood cells.
Thirty-two dogs underwent 2 hours of ligation of the left anterior descending coronary artery followed by 20 minutes of regional blood cardioplegic reperfusion on bypass. Ten dogs received only the blood cardioplegic solution (containing its endogenous free radical scavengers); five received initial blood cardioplegia (5 minutes) with endogenous free radical scavengers (catalase and glutathione peroxidase) blocked by aminotriazole and N-ethylmaleimide, respectively; 12 received initial crystalloid cardioplegic solution oxygenated by room air (oxygen tension = 150 mm Hg); seven without and five with exogenous free radical scavengers (superoxide dismutase, catalase, coenzyme Q10); five received initial deoxygenated crystalloid cardioplegic solution (oxygen tension = 6 mm Hg); and five received deoxygenated crystalloid cardioplegic solution.
Blood cardioplegia with endogenous free radical scavengers produced the best recovery of systolic shortening (69% systolic shortening) and resulted in the least histochemical damage (11% triphenyltetrazolium chloride nonstaining). The worst recovery and most damage occurred if blood cardioplegia was preceded by oxygenated crystalloid cardioplegia (3% systolic shortening, 48% triphenyltetrazolium chloride nonstaining; p less than 0.05 versus blood cardioplegia) or if free radical scavengers were blocked in the initial period of blood cardioplegia (3% systolic shortening, 41% triphenyltetrazolium chloride nonstaining; p less than 0.05 versus blood cardioplegia). Conversely, deoxygenation or supplementation of oxygenated crystalloid cardioplegic solution with exogenous free radical scavengers restored 60% systolic shortening (p less than 0.05 versus oxygenated crystalloid cardioplegia) and 54% systolic shortening (p less than 0.05 versus oxygenated crystalloid cardioplegia) and reduced damage to 34% and 21% (both p less than 0.05 versus oxygenated crystalloid cardioplegia).
Blood cardioplegic solutions containing their own endogenous free radical scavengers are superior to crystalloid cardioplegic solutions, because they limit oxygen-mediated perfusion damage and restore contractile function. Initial crystalloid cardioplegic washout negates the salutary effect of blood cardioplegia. Exogenous free radical scavenger supplementation or deoxygenation of the cardioplegic reperfusate is necessary only if crystalloid cardioplegia is used.
缺血后损伤部分由氧自由基介导的损伤引起。本研究将表明：（1）含室内空气氧的晶体心脏停搏液是有害的，因为它缺乏自由基清除剂；（2）血液心脏停搏液可限制损伤，因为它在红细胞中含有内源性自由基清除剂。
32只犬接受左前降支冠状动脉结扎2小时，随后在体外循环下进行20分钟的区域性血液心脏停搏液再灌注。10只犬仅接受血液心脏停搏液（含有其内源性自由基清除剂）；5只犬最初接受血液心脏停搏液（5分钟），其中内源性自由基清除剂（过氧化氢酶和谷胱甘肽过氧化物酶）分别被氨基三唑和N - 乙基马来酰亚胺阻断；12只犬最初接受经室内空气氧合的晶体心脏停搏液（氧张力 = 150 mmHg）；7只犬未使用外源性自由基清除剂，5只犬使用了外源性自由基清除剂（超氧化物歧化酶、过氧化氢酶、辅酶Q10）；5只犬最初接受脱氧晶体心脏停搏液（氧张力 = 6 mmHg）；5只犬接受脱氧晶体心脏停搏液。
含有内源性自由基清除剂的血液心脏停搏液产生了最佳的心收缩期缩短恢复（心收缩期缩短69%），且导致的组织化学损伤最少（11%的三苯基四氮唑氯化物不着色）。如果在血液心脏停搏液之前使用氧合晶体心脏停搏液（心收缩期缩短3%，48%的三苯基四氮唑氯化物不着色；与血液心脏停搏液相比，p < 0.05），或者如果在血液心脏停搏液的初始阶段自由基清除剂被阻断（心收缩期缩短3%，41%的三苯基四氮唑氯化物不着色；与血液心脏停搏液相比，p < 0.05），则恢复最差且损伤最大。相反，脱氧或用外源性自由基清除剂补充氧合晶体心脏停搏液可使心收缩期缩短恢复到60%（与氧合晶体心脏停搏液相比，p < 0.05）和54%（与氧合晶体心脏停搏液相比，p < 0.05），并将损伤减少到34%和21%（两者与氧合晶体心脏停搏液相比，p < 0.05）。
含有自身内源性自由基清除剂的血液心脏停搏液优于晶体心脏停搏液，因为它们可限制氧介导的灌注损伤并恢复收缩功能。最初的晶体心脏停搏液冲洗会抵消血液心脏停搏液的有益作用。仅在使用晶体心脏停搏液时才需要补充外源性自由基清除剂或对心脏停搏液再灌注液进行脱氧处理。
