SECONDARY ISCHEMIA IN RABBIT SKIN FLAPS - THE ROLES PLAYED BY THROMBOXANE AND FREE-RADICALS
SECONDARY ISCHEMIA IN RABBIT SKIN FLAPS - THE ROLES PLAYED BY THROMBOXANE AND FREE-RADICALS
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DOI：
10.1042/cs0800235
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发表时间：
1991-03-01
期刊：
影响因子：
6
通讯作者：
OBRIEN, BM
中科院分区：
文献类型：
--
作者：
KNIGHT, KR;ANGEL, MF;OBRIEN, BM
1.本实验研究了兔皮瓣缺血的生化机制，首先缺血2 h，然后再缺血24 h，再缺血4 h。在继发性缺血期间，皮瓣发生完全缺血（动脉和静脉血供闭塞）或部分缺血（仅静脉闭塞）。其中一些皮瓣在再灌注时用自由基清除剂超氧化物歧化酶（EC 1.15.1.1）和/或血栓素合成酶抑制剂UK-38，485.2处理。再灌注30分钟后，超氧化物歧化酶治疗显着降低血液血栓素水平，升高缺血。超氧化物歧化酶还降低了组织中丙二醛和黄嘌呤氧化酶的水平，这是自由基损伤的指标，并恢复了超氧化物歧化酶的耗竭组织水平。UK-38，485治疗未能显著改变这些组织自由基参数中的任何一个，尽管该药剂显著降低血液血栓素水平。联合超氧化物歧化酶和UK-38，485治疗在任何参数方面都没有显著优于单独治疗。部分缺血导致组织自由基和血液血栓素水平始终高于总缺血。因此，部分缺血似乎比完全缺血导致更大的自由基损伤。这些结果是一致的假设，血栓素作为一个调解人的自由基损伤的缺血性变化内皮瓣。
1. Biochemical mechanisms of ischaemia were investigated in rabbit skin flaps subjected to 2 h of primary ischaemia then, 24 h later, to 4 h of secondary ischaemia. During secondary ischaemia, flaps underwent either total ischaemia (arterial and venous blood supply occluded) or partial ischaemia (vein only occluded). Some of these flaps were treated at the time of reperfusion with the freeradical scavenger superoxide dismutase (EC 1.15.1.1) and/or the thromboxane synthetase inhibitor UK-38,485.2. After 30 min of reperfusion, superoxide dismutase treatment significantly reduced blood thromboxane levels, elevated during ischaemia. Superoxide dismutase also reduced tissue levels of malonyldialdehyde and xanthine oxidase, indicators of free-radical damage, and restored the depleted tissue levels of superoxide dismutase.3. UK-38,485 treatment failed to significantly alter any of these tissue free-radical parameters, although this agent significantly reduced blood thromboxane levels.4. Combined superoxide dismutase plus UK-38,485 treatment was not significantly better than either treatment alone with respect to any parameter.5. Partial ischaemia led to consistently higher levels of tissue free radicals and blood thromboxane than did total ischaemia. Thus partial ischaemia appears to result in greater free-radical damage than total ischaemia.6. These results are consistent with the hypothesis that thromboxane acts as a mediator for free-radical damage in the ischaemic changes within the flap.