Zar H A, Tanigawa K, Kim Y M, Lancaster J R
University of North Carolina, Chapel Hill 27599, USA.
Free Radic Biol Med. 1998 Aug;25(3):255-64. doi: 10.1016/s0891-5849(98)00032-x.
In this investigation, we used chemiluminescence to study the ability of increasing durations of ischemia (1, 2, or 2.5 h) to induce enhanced generation of reactive oxygen species in a crystalloid perfused rat liver model. To evaluate the effect of reactive oxygen species generation upon the development of the postischemic hypoperfusion, hepatic vascular resistance was simultaneously monitored. One hour of ischemia did not produce sustained reactive oxygen species generation or development of no-reflow. Two hours of ischemia did not result in sustained reactive oxygen species generation but did produce no-reflow. Sustained reactive oxygen production was achieved after 2.5 h of ischemia and was accompanied by the development of no-reflow. We found that 2.5 h of ischemia is the threshold for sustained lipid peroxidation. Both lipid peroxidation and no-reflow could be mitigated through the administration of superoxide dismutase. Superoxide dismutase could reduce the amount of cell injury due to the enhanced lipid peroxidation induced by 2.5 h of ischemia. Limitation of reactive oxygen species generation to a critical threshold, either by restricting the duration of ischemia or by pharmacological intervention, may be an important means of preventing further cellular injury through no-reflow and lipid peroxidation.
在本研究中，我们利用化学发光法，在晶体灌注大鼠肝脏模型中，研究延长缺血时间（1、2或2.5小时）诱导活性氧生成增加的能力。为评估活性氧生成对缺血后低灌注发展的影响，同时监测肝血管阻力。1小时的缺血未产生持续性活性氧生成或无复流现象。2小时的缺血未导致持续性活性氧生成，但产生了无复流现象。缺血2.5小时后实现了持续性活性氧生成，并伴有无复流现象的发展。我们发现2.5小时的缺血是持续性脂质过氧化的阈值。脂质过氧化和无复流现象均可通过给予超氧化物歧化酶得到缓解。超氧化物歧化酶可减少因2.5小时缺血诱导的脂质过氧化增强所导致的细胞损伤量。通过限制缺血时间或药物干预将活性氧生成限制在临界阈值，可能是预防因无复流和脂质过氧化导致进一步细胞损伤的重要手段。
