Oxidative stress in ischemia-reperfusion injury: assessment by three independent biochemical markers.
Oxidative stress in ischemia-reperfusion injury: assessment by three independent biochemical markers.
复制标题
缺血再灌注损伤中的氧化应激：通过三种独立的生化标记物进行评估。
DOI：
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发表时间：
2000
期刊：
影响因子：
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通讯作者：
S. Santini
中科院分区：
文献类型：
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作者：
S. Rigattieri;A. Buffon;V. Ramazzotti;A. Mordente;F. Crea;A. Maseri;B. Giardina;S. Santini
背景
氧化应激在缺血再灌注损伤中起关键作用，引起组织脂质和蛋白质过氧化。然而，短暂的缺血发作是否足以引起可检测的氧化应激在人类中存在争议，因为迄今为止在经皮腔内冠状动脉成形术（PTCA）的设置中使用的生化标记物给出了相互矛盾的结果。
方法
我们测定了5例接受PTCA的患者在单次球囊扩张持续115 +/- 38 s（t0）、1 min（t1）、5 min（t5）前主动脉和心大静脉血中脂质过氧化氢（ROOHs）、共轭二烯（CD）和总自由基捕获抗氧化能力（TRAP），这三种不同的氧化应激独立标志物。球囊回缩后15 min（t15）（组1）。同时测定5例二尖瓣病变患者（第2组）主动脉和心大静脉血ROOH和CD。
结果
在第1组中，与t0相比，t1时的心大静脉ROOH和CD水平分别增加了219%和79%（p < 0.01）;这种急剧和一致的增加持续到t15（与t0相比，分别为+189%和+63%; p < 0.01）。在t0时，心脏大静脉的TRAP水平显著低于主动脉水平，并且在t1时表现出进一步降低。在t0时，第1组和第2组之间未观察到ROOH和CD的主动脉和心大静脉水平存在显著差异。
结论
我们使用的三种方法显示出显着的敏感性检测缺血后再灌注损伤的心脏静脉血，并可能是有用的检测缺血再灌注损伤的微血管性心绞痛的小病灶。
BACKGROUND
Oxidative stress plays a key role in ischemia-reperfusion injury, causing peroxidation of tissue lipids and proteins. However, it is debated whether brief ischemic episodes are sufficient to cause detectable oxidative stress in humans, since biochemical markers used so far in the setting of percutaneous transluminal coronary angioplasty (PTCA) gave conflicting results.
METHODS
We determined lipid hydroperoxides (ROOHs), conjugated dienes (CD) and total radical-trapping antioxidant capacity (TRAP), three different independent markers of oxidative stress, in aortic and great cardiac vein blood of 5 patients undergoing PTCA before a single balloon inflation lasting 115 +/- 38 s (t0), and 1 min (t1), 5 min (t5), 15 min (t15) after balloon deflation (Group 1). ROOHs and CD were also determined in aortic and great cardiac vein blood of 5 patients with mitral valve disease (Group 2).
RESULTS
In Group 1, great cardiac vein levels of ROOHs and CD at t1 increased by 219% and 79%, respectively, compared to t0 (p < 0.01); this sharp and consistent increase persisted up to t15 (+189% and +63%, respectively, compared to t0; p < 0.01). Great cardiac vein levels of TRAP were significantly lower than aortic levels at t0, and exhibited a further decrease at tl. No significant differences in aortic and great cardiac vein levels of ROOHs and CD at t0 were observed between Group 1 and Group 2.
CONCLUSIONS
The three methods we used showed a remarkable sensitivity for the detection of post-ischemic reperfusion injury in cardiac venous blood and may be useful for detecting small foci of ischemia-reperfusion injury in microvascular angina.