ZINC IMPROVES POSTISCHEMIC RECOVERY OF ISOLATED RAT HEARTS THROUGH INHIBITION OF OXIDATIVE STRESS
ZINC IMPROVES POSTISCHEMIC RECOVERY OF ISOLATED RAT HEARTS THROUGH INHIBITION OF OXIDATIVE STRESS
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DOI：
10.1152/ajpheart.1994.266.6.h2497
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发表时间：
1994-06-01
影响因子：
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通讯作者：
TORTOLANI, AJ
中科院分区：
文献类型：
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作者：
POWELL, SR;HALL, D;TORTOLANI, AJ
我们研究了锌对缺血后离体大鼠心脏的保护作用。用含或不含双组氨酸锌的Krebs-Henseleit缓冲液灌注心脏，进行20分钟的“无血流”恒温全局缺血。用0、10、20或30 μ M锌进行缺血前和缺血后处理可导致缺血后功能的浓度依赖性增强，表现为舒张末压降低（分别为37 +/- 3、25 +/- 5、17 +/- 5和8 +/- 2 mmHg），收缩压恢复增加（分别为41 +/- 6、59 +/- 17、76 +/- 18和87 +/- 16 mmHg）和最大压力上升率（+dP/dt(max)）；分别为823 +/- 141,1413 +/- 396,1700 +/- 450和2157 +/- 407 mmHg/s)。乳酸脱氢酶从心脏流出量减少（峰值分别为1002%、840%、580%和440%）。只有缺血前治疗能产生中等程度的保护作用，而从再灌注开始治疗会加重缺血后损伤。在整个实验过程中灌注锌的心脏，延长缺血前治疗间隔进一步促进缺血后恢复。用水杨酸盐作为诱捕剂。OH，锌几乎消除了该制剂中通常观察到的该物种的早期缺血后“爆发”。原子吸收研究表明，在再灌注期结束时，用30 μ M锌处理的心脏比对照心脏含铜量少27%。在对照心脏中，电镜显示线粒体肿胀，内部基质密度明显下降，而锌处理后的心脏形态基本正常。这些研究表明，锌具有心脏细胞保护特性，并支持这种金属可以减少的概念。通过影响铜的反应性来形成OH。
We studied the cardiac protective qualities of zinc in the postischemic isolated rat heart. Hearts, perfused with Krebs-Henseleit buffer with or without zinc-bis-histidinate, were subjected to 20 min of ''no-flow'' normothermic global ischemia. Pre- and postischemic treatment with 0, 10, 20, or 30 mu M zinc resulted in concentration-dependent enhancement of postischemic function as evidenced by decreased end-diastolic pressure (37 +/- 3, 25 +/- 5, 17 +/- 5, and 8 +/- 2 mmHg, respectively) and increased recovery of developed systolic pressure (41 +/- 6, 59 +/- 17, 76 +/- 18, and 87 +/- 16 mmHg, respectively) and maximum rate of rise in pressure (+dP/dt(max); 823 +/- 141, 1,413 +/- 396, 1,700 +/- 450, and 2,157 +/- 407 mmHg/s, respectively) as well. as decreased lactate dehydrogenase efflux from the hearts (peak: 1,002%, 840%, 580%, and 440%, respectively). Only preischemic treatment resulted in an intermediate protective effect, whereas treatment starting at reperfusion worsened postischemic damage. In hearts perfused with zinc throughout the experiment, prolongation of the preischemic treatment interval further enhanced postischemic recovery. With the use of salicylate as a trap for .OH, it was determined that zinc virtually eliminated the early postischemic ''burst'' of this species normally observed in this preparation. Atomic absorption studies demonstrated that hearts treated with 30 mu M zinc contained 27% less copper than control hearts by the end of the reperfusion period. In control hearts, electron microscopy revealed swollen mitochondria with marked loss of inner matrix density, whereas morphology of postischemic zinc-treated hearts was essentially normal. These studies indicate that zinc possesses cardiac cytoprotective qualities and support the concept that this metal can decrease .OH formation by affecting copper reactivity.