Chambers D J, Braimbridge M V, Hearse D J
Rayne Institute, St. Thomas Hospital, London, UK.
Eur J Cardiothorac Surg. 1987;1(2):80-90. doi: 10.1016/1010-7940(87)90016-9.
The isolated perfused working rat heart model of cardiopulmonary bypass was used to assess whether (a) allopurinol pretreatment enhances resistance to normothermic (30 min) or hypothermic (4 h) ischemia; (b) addition of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) to cardioplegic and/or reperfusion solutions are protective; (c) any protective effects are additive. With normothermic ischemia, allopurinol pretreatment improved recovery of aortic flow from its control value of 25 +/- 3% to 48 +/- 6% (P less than 0.05). Similarly, SOD plus CAT used during both ischemia and reperfusion improved recovery of aortic flow from a control value of 28 +/- 4% to 48 +/- 6% (P less than 0.05). However, various combinations of the two types of intervention afforded no additive protection. Under hypothermic (21 degrees C) conditions, allopurinol pretreatment was not effective, whereas SOD and CAT added during ischemia and reperfusion improved recovery of aortic flow from its control value of 53 +/- 4% to 69 +/- 5% (P less than 0.05). This value was similar to allopurinol pretreatment and SOD plus CAT added during ischemia and reperfusion (69 +/- 6%: P less than 0.05). These results provide further evidence that reperfusion-induced free radical formation may adversely affect postischemic recovery of function. The absence of an additive effect suggests a common mechanism of action, which is likely to involve the free radical-generating enzyme xanthine oxidase; however, other mechanisms may exist. Our results further support the use of antifree radical intervention in conjunction with cardioplegia to protect the heart during ischemia and reperfusion.
采用体外循环大鼠离体灌注工作心脏模型，评估：(a) 别嘌呤醇预处理是否增强对常温（30分钟）或低温（4小时）缺血的耐受性；(b) 在心脏停搏液和/或再灌注液中添加抗氧化酶超氧化物歧化酶（SOD）和过氧化氢酶（CAT）是否具有保护作用；(c) 任何保护作用是否具有相加性。在常温缺血时，别嘌呤醇预处理使主动脉血流恢复率从对照值25±3%提高到48±6%（P<0.05）。同样，在缺血和再灌注期间使用SOD加CAT使主动脉血流恢复率从对照值28±4%提高到48±6%（P<0.05）。然而，两种干预方式的不同组合未产生相加性保护作用。在低温（21℃）条件下，别嘌呤醇预处理无效，而在缺血和再灌注期间添加SOD和CAT使主动脉血流恢复率从对照值53±4%提高到69±5%（P<0.05）。该值与别嘌呤醇预处理以及在缺血和再灌注期间添加SOD加CAT的结果相似（69±6%：P<0.05）。这些结果进一步证明，再灌注诱导的自由基形成可能对缺血后功能恢复产生不利影响。缺乏相加效应提示存在共同的作用机制，可能涉及产生活性氧的黄嘌呤氧化酶；然而，也可能存在其他机制。我们的结果进一步支持在心脏停搏时联合使用抗自由基干预措施，以在缺血和再灌注期间保护心脏。
