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人超氧化物歧化酶在大鼠心肌缺血两种再灌注模型中的心脏保护作用

Cardioprotective actions of human superoxide dismutase in two reperfusion models of myocardial ischaemia in the rat.

作者信息

Aoki N, Bitterman H, Brezinski M E, Lefer A M

机构信息

Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.

出版信息

Br J Pharmacol. 1988 Nov;95(3):735-40. doi: 10.1111/j.1476-5381.1988.tb11699.x.

DOI:10.1111/j.1476-5381.1988.tb11699.x
PMID:3207990
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1854226/
Abstract
  1. In rats under ether anaesthesia, the left coronary artery was ligated and reperfused after 10 min of ischaemia. Forty-eight hours later the myocardium was analyzed for creatine kinase (CK) activity. 2. Human superoxide dismutase (h-SOD) given 1 min after occlusion and again 6 h later significantly improved survival and retarded the loss of myocardial CK. 3. In rat isolated hearts perfused at 15% of normal flow for 30 min followed by re-establishment of normal flow for 20 min, perfusion pressure increased by 72% and myocardial CK decreased by 44%. No significant changes occurred in wet-to-dry heart weight ratio. 4. Administration of h-SOD at 2.5 or 5.0 mg, significantly attenuated the elevated post-ischaemic perfusion pressure and the loss of myocardial CK activity in rat perfused hearts. 5. h-SOD appears to be an effective anti-ischaemic agent in the intact animal as well as the isolated perfused heart of the rat subjected to low flow followed by reperfusion at normal flow. The mechanism of this cardioprotective effect is not totally dependent upon the formed elements of the blood, but may be partially due to a direct cytoprotective effect.
摘要
  1. 在乙醚麻醉的大鼠中,结扎左冠状动脉并在缺血10分钟后再灌注。48小时后分析心肌的肌酸激酶(CK)活性。2. 在闭塞后1分钟及6小时后再次给予人超氧化物歧化酶(h-SOD),可显著提高存活率并延缓心肌CK的损失。3. 在以正常流量的15%灌注30分钟然后恢复正常流量20分钟的大鼠离体心脏中,灌注压力增加72%,心肌CK降低44%。湿重与干重之比无显著变化。4. 给予2.5或5.0毫克的h-SOD可显著减轻大鼠灌注心脏缺血后升高的灌注压力和心肌CK活性的损失。5. h-SOD似乎是完整动物以及经历低流量后以正常流量再灌注的大鼠离体灌注心脏中的一种有效的抗缺血剂。这种心脏保护作用的机制并不完全依赖于血液的有形成分,而可能部分归因于直接的细胞保护作用。

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本文引用的文献

1
Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog.犬心肌缺血再灌注时的白细胞毛细血管阻塞
Am J Pathol. 1983 Apr;111(1):98-111.
2
Canine myocardial reperfusion injury. Its reduction by the combined administration of superoxide dismutase and catalase.犬心肌再灌注损伤。超氧化物歧化酶和过氧化氢酶联合给药对其的减轻作用。
Circ Res. 1984 Mar;54(3):277-85. doi: 10.1161/01.res.54.3.277.
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Leukotrienes and the cardiovascular system.白三烯与心血管系统。
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Superoxide dismutase. An enzymic function for erythrocuprein (hemocuprein).超氧化物歧化酶。红细胞铜蛋白(血铜蛋白)的酶功能。
J Biol Chem. 1969 Nov 25;244(22):6049-55.
6
An improved procedure for serum creatine phosphokinase determination.一种改进的血清肌酸磷酸激酶测定方法。
J Lab Clin Med. 1967 Apr;69(4):696-705.
7
Myocardial reperfusion: a double-edged sword?心肌再灌注:一把双刃剑?
J Clin Invest. 1985 Nov;76(5):1713-9. doi: 10.1172/JCI112160.
8
Enhancement of recovery of myocardial function by oxygen free-radical scavengers after reversible regional ischemia.可逆性局部缺血后氧自由基清除剂对心肌功能恢复的促进作用。
Circulation. 1985 Oct;72(4):915-21. doi: 10.1161/01.cir.72.4.915.
9
Involvement of hydrogen peroxide and hydroxyl radical in the 'oxygen paradox': reduction of creatine kinase release by catalase, allopurinol or deferoxamine, but not by superoxide dismutase.过氧化氢和羟自由基在“氧悖论”中的作用:过氧化氢酶、别嘌呤醇或去铁胺可减少肌酸激酶释放,但超氧化物歧化酶无此作用。
J Mol Cell Cardiol. 1985 Jul;17(7):675-84. doi: 10.1016/s0022-2828(85)80067-5.
10
Failure of superoxide dismutase and catalase to alter size of infarction in conscious dogs after 3 hours of occlusion followed by reperfusion.在阻断3小时后再灌注的清醒犬中,超氧化物歧化酶和过氧化氢酶未能改变梗死灶大小。
Circulation. 1986 May;73(5):1065-76. doi: 10.1161/01.cir.73.5.1065.