摘要

This study used an electrochemical O-2(-center dot) sensor to investigate the effects of hyperoxia on generation of the superoxide radical (O-2(-center dot)) in the jugular vein during forebrain I/R in rats. Twenty-eight male Wistar rats were allocated to a sham group (n = 7; sham-treated rats with inspired oxygen fraction [FIO2] of 0.4), a hemorrhagic shock and reperfusion (HS/R) group (n = 7; HS without carotid artery occlusion and reperfusion with FIO2 of 0.4), a normoxia group (n = 7; forebrain ischemia produced by bilateral carotid arteries occlusion with HS and reperfusion with FIO2 of 0.4), and a hyperoxia group (n = 7; forebrain ischemia with FIO2 of 0.4 and reperfusion with FIO2 of 1.0). The jugular venous O-2(-center dot) current was measured for 10 min during forebrain ischemia and for 120 min after reperfusion. The O-2(-center dot) current increased gradually during forebrain ischemia in the three groups other than the sham group. Immediately after reperfusion, the current showed a marked increase in the normoxia group and a pronounced decrease in the hyperoxia group. Levels of brain and plasma malondialdehyde, high-mobility group box 1 protein, and intercellular adhesion molecule 1 were significantly attenuated in the hyperoxia group relative to those in the normoxia group. In conclusion, hyperoxia suppressed jugular venous O-2(-center dot) generation and malondialdehyde, high-mobility group box 1, and intercellular adhesion molecule 1 in the brain and plasma in the acute phase of cerebral I/R. Thus, the administration of 100% oxygen immediately after reperfusion suppresses oxidative stress and early inflammation in cerebral I/R.

  • 出版日期2010-9