Cardioplegia-induced damage to ischemic immature myocardium is independent of oxygen availability.
Cardioplegia-induced damage to ischemic immature myocardium is independent of oxygen availability.
复制标题
心脏停搏液引起的对缺血性未成熟心肌的损伤与氧气的可用性无关。
DOI：
10.1016/0003-4975(90)91125-u
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Olinger,GN
中科院分区：
文献类型：
--
作者：
Baker,JE;Boerboom,LE;Olinger,GN
低温药物心脏停搏液在保护缺血成人心脏方面的已知益处可能不适用于儿童。低温Krebs-Henseleit碳酸氢盐缓冲液对缺血未成熟兔心的保护作用优于低温St.托马斯Ⅱ停搏液。我们研究了缺血前灌注液中氧的可用性是否是与缺血前即刻用St.托马斯II溶液相比，用Krebs缓冲液灌注的未成熟（7- 10天）心脏对缺血耐受性增加的原因。在“工作”模式下获得缺血前对照数据后，我们用低温（14 °C）Krebs缓冲液或低温St.托马斯II溶液（含0%、25%或95%氧气）灌注心脏（每组n = 8）3分钟。随后在14 °C下进行2小时的全脑缺血。心脏在Langendorff模式下再灌注15分钟，在工作模式下再灌注35分钟，并测量功能恢复。在缺血前氧浓度为0%、25%和95%时，缺血期间仅用低温保护的心脏的主动脉血流恢复分别为缺血前值的74% ± 9%、82% ± 4%和99% ± 2%。在低温加停搏液保护的心脏中，该值分别为69% ± 6%、72% ± 3%和86% ± 5%。因此，在相同的氧浓度下，与低温加心脏停搏液相比，单独低温保护的心脏缺血后功能恢复更好。我们的结论是氧供应以外的因素是负责圣托马斯II解决方案对缺血未成熟兔心脏的损害作用。
The known benefits of hypothermic pharmacological cardioplegia in protecting the ischemic adult heart may not extend to children. Protection of the ischemic immature rabbit heart with hypothermic Krebs-Henseleit bicarbonate buffer is better than with hypothermic St. Thomas' II cardioplegic solution. We investigated whether the availability of oxygen in the preischemic perfusate is responsible for the increased tolerance to ischemia of immature (7- to 10-day-old) hearts perfused with Krebs buffer in comparison with St. Thomas' II solution immediately before ischemia. After obtaining preischemic control data in the “working” mode, we perfused hearts (n = 8 per group) for 3 minutes with hypothermic (14 °C) Krebs buffer or hypothermic St. Thomas' II solution saturated with 0%, 25%, or 95% oxygen. This was followed by 2 hours of global ischemia at 14 °C. Hearts were reperfused for 15 minutes in the Langendorff mode and 35 minutes in the working mode, and recovery of function was measured. For preischemic oxygen concentrations of 0%, 25%, and 95%, recovery of aortic flow in hearts protected by hypothermia alone during ischemia was 74% ± 9%, 82% ± 4%, and 99% ± 2% of preischemic values, respectively. In hearts protected by hypothermia plus cardioplegia, the values were 69% ± 6%, 72% ± 3%, and 86% ± 5%, respectively. Thus, at equal oxygen concentrations, recovery of postischemic function was better in hearts protected by hypothermia alone compared with hypothermia plus cardioplegia. We conclude that factors other than oxygen availability are responsible for the damaging effect of St. Thomas' II solution on the ischemic immature rabbit heart.