| Na^＋—K^＋—ATP酶抑制与心肌缺血后再灌注性损伤 |
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| 引用本文： | 赵廷存,徐海.Na^＋—K^＋—ATP酶抑制与心肌缺血后再灌注性损伤[J].中国应用生理学杂志,1993,9(1):16-19. |
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| 作者姓名： | 赵廷存 徐海 |
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| 作者单位： | 北京医科大学病理生理学教研室，北京医科大学病理生理学教研室，北京医科大学病理生理学教研室 北京 100083，北京 100083，北京 100083 |
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| 摘 要： | 在离体大鼠心脏灌流模型上,观察细胞内高钠对心肌缺血后再灌注性损伤的影响。在低灌流过程中,给予Na~ -K~ -ATP酶抑制剂哇巴因造成细胞内高Na~ ,可加重缺血后再灌注心脏的血液动力学障碍;增加心肌组织丙二醛含量及冠脉流出液中乳酸脱氢酶的活性;降低线粒体及胞浆液中谷胱甘肽过氧化物酶活力;并使心肌组织中Ca~(2 )超负荷及K~ 丢失严重。因此,细胞内高Na~ 可能是心肌缺血后再灌注损伤的基础。
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| 关 键 词： | Na~ 超负荷 再灌注性损伤 哇巴因 Na~ -K~ -ATP酶 |
Na~ -K~ -ATPase INHIBITION AND POST-ISCHEMIC REPERFUSION INJURY |
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| Zhao Tingcun,Xu Hai,Shi Anyun.Na~ -K~ -ATPase INHIBITION AND POST-ISCHEMIC REPERFUSION INJURY[J].Chinese Journal of Applied Physiology,1993,9(1):16-19. |
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| Authors: | Zhao Tingcun Xu Hai Shi Anyun |
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| Abstract: | The detrimental effects of ouabain on post-ischemic myocardium were observed in the model of ischemic-reperfusion injury in isolated rat hearts. Ouabain was added to anoxic Krebs-Henseleit solution during low flow perfusion. As compared with the control group, ouabain caused additional increase in Na after reperfusion, associated with depression of ventricular function, Ca2 overload, loss of K , increase in MDA contenty and LDH activity and decrease in GSH-Px activity. These results suggest that Na overload induced by ouabain may play a certain role in the mechanism of ischemic reperfusion injury. |
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| Keywords: | Na overload reperfusion injury ouabain Na -K -ATPase |
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