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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.

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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