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。
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.
出处
《中国应用生理学杂志》
CAS
CSCD
1993年第1期16-19,共4页
Chinese Journal of Applied Physiology
关键词
钠
钙
ATP酶
心肌缺血
再灌注损伤
Na+ overload
reperfusion injury
ouabain
Na+-K+-ATPase
