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首页> 外文期刊>Biochemistry >Allopurinol Enhances Adenine Nucleotide Levels and Improves Myocardial Function inIsolated Hypoxic Rat Heart
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Allopurinol Enhances Adenine Nucleotide Levels and Improves Myocardial Function inIsolated Hypoxic Rat Heart

机译：别嘌呤醇增强缺氧大鼠心脏的腺嘌呤核苷酸水平并改善心肌功能

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Allopurinol, a competitive inhibitor of xanthine oxidase, was found to have a protective effect on ischemic myocardium. Its mechanism of action is still controversial. We used Langendorff isolated rat heart preparation to test the hypothesis that allopurinol could maintain a level of the adenine nucleotide pool (ATP, ADP, and AMP) that would protect and improve the functional activity of the heart during a period of hypoxia. Hearts were initially perfused for 30 min until steady state was attained. This was foUowed by 20 min of experimental perfusion divided into 5 min of control perfusion followed by 15 min of hypoxic perfusion with or without allopurinol in the perfusate. Hearts were quick-frozen and enzymati-cally analyzed for adenine nucleotides and creatine phosphate at the end of the hypoxic period. Left ventricular pressure, heart rate, and coronary flow were measured in all preparations. Allopurinol (0.1 mM) treated hearts had greater levels of ATP ( 12.3 +- 0.8 vs. 9.3 +- 0.8 #mu#mol/g dry weight; p < 0.01). This improvement occurred in the presence as well as the absence of glucose. Total adenine nucleotides improved from 17 +- 1 to 20.3 +- 2.4 #mu#mol/g dry weight (p < 0.01). This improvement also occurred in the presence as well as in the absence of glucose in the perfusate. It also improved cell energy state significantly in the presence as well as the absence of glucose. There was insignificant change in creatine phosphate. Allopurinol improved left ventricular pressure from 38 +- 7% to 55 +- 9% (p < 0.002) in the presence of glucose and from 8 +- 3% to 27 +- 6.3% (p < 0.001) in the absence of glucose. Coronary flow improved from 110 +- 5% to 120 +- 8% (p < 0.04) in the presence of glucose. These results support the suggestion that allopurinol at 0.1 mM exerts its protective effect on rat heart during hypoxia by enhancing the adenine nucleotide pool.
机译：发现黄嘌呤氧化酶的竞争性抑制剂别嘌醇对缺血性心肌有保护作用。其作用机理仍存在争议。我们使用Langendorff分离的大鼠心脏制剂来测试以下假设：别嘌呤醇可以维持一定水平的腺嘌呤核苷酸池（ATP，ADP和AMP），该水平将在缺氧期间保护和改善心脏的功能活性。最初将心脏灌注30分钟，直到达到稳定状态。这是通过20分钟的实验灌注分为5分钟的对照灌注，然后是灌注液中有或没有别嘌呤醇的低氧灌注15分钟。在缺氧期结束时，将心脏速冻并通过酶法分析腺嘌呤核苷酸和磷酸肌酸。在所有制剂中均测量左心室压力，心率和冠状动脉血流。用别嘌醇（0.1 mM）处理的心脏具有更高的ATP水平（12.3±0.8 vs. 9.3±0.8＃mu＃mol / g干重; p <0.01）。在存在和不存在葡萄糖的情况下都会发生这种改善。总腺嘌呤核苷酸从17 +/- 1提高到20.3 +/- 2.4＃mu＃mol / g干重（p <0.01）。在灌注液中存在和不存在葡萄糖的情况下也发生了这种改善。在存在和不存在葡萄糖的情况下，它也显着改善了细胞能量状态。磷酸肌酸变化不大。在有葡萄糖的情况下，别嘌呤醇将左心室压力从38 +-7％提高到55 +-9％（p <0.002），在没有葡萄糖的情况下将左心室压力从8 +-3％提高到27 +-6.3％（p <0.001） 。在葡萄糖存在下，冠状动脉血流从110±5％提高到120±8％（p <0.04）。这些结果支持以下建议：0.1 mM的别嘌呤醇可通过增强腺嘌呤核苷酸库在缺氧时对大鼠心脏发挥保护作用。

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