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急性缺血的主要生化后果是细胞缺氧致线粒体抑制和缺乏代谢底物葡萄糖致ATP合成抑制。已证明氧自由基是缺血器官恢复灌流后发生损伤的重要介质。作者通过模拟活体内急性缺血条件的体外“化学缺血”模型,研究在缺血情况下发生的细胞代谢抑制是否加重其后遭受的氧化剂损伤。牛肺动脉上皮细胞混悬液加无糖缓冲液和(或)线粒体抑制剂(650nM寡霉素或4mM
The main biochemical consequences of acute ischemia are mitochondrial inhibition of cell hypoxia and inhibition of ATP synthesis by the lack of metabolic substrate glucose. It has been demonstrated that oxygen free radicals are important mediators of injury following the recovery of ischemic organs from perfusion. By examining in vitro “chemo-ischemia” models of acute ischemic conditions in vivo, we investigated whether cellular metabolic inhibition that occurs under ischemic conditions aggravates subsequent oxidant damage. Bovine Pulmonary Artery Epithelial Cell Suspension plus Sugarless Buffer and / or Mitochondrial Inhibitors (650 nM oligomycin or 4 mM