Berg Kirsti, Jynge Per, Bjerve Kristian, Skarra Sissel, Basu Samar, Wiseth Rune
Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway.
Free Radic Res. 2005 Jun;39(6):629-36. doi: 10.1080/10715760400028027.
In acute myocardial infarction (AMI) treated with percutaneous coronary intervention (PCI), myocardial injury results from complex processes during both ischemia and reperfusion. Release of reactive oxygen species (ROS) may contribute to the accumulated myocardial damage.
To examine by frequent sampling of peripheral blood oxidative stress and early inflammation in patients undergoing primary PCI for AMI. Secondly, to assess whether a correlation exists between these parameters and the extent of myocardial damage.
Sixteen patients undergoing primary PCI within 6 h of AMI onset were included. Peripheral blood was sampled at start of procedure (t0) and repeatedly over 24 h following reperfusion. Main plasma analyses were: 8-iso-PGF2alpha (oxidative stress), 15-keto-dihydro-PGF2alpha (cyclooxygenase-mediated inflammation); and troponin-T (myocardial injury). Additional analyses included: total antioxidant status (TAS); vitamins; hsCRP and lipids.
8-Iso-PGF2alpha increased following restoration of blood flow, returned to t0 values after 3 h and was reduced below t0 the following day. TAS decreased significantly from t0 to the next day. There was no significant correlation between 8-iso-PGF2alpha and troponin T values. 15-Keto-dihydro-PGF2alpha was elevated during the first hour. There was a major rise in hsCRP after 24 h.
Following reperfusion by primary PCI in AMI, oxidative stress and an inflammatory response are induced immediately. A rise in 8-iso-PGF2a during ischemia indicate that ROS generation may also take place during severely reduced coronary blood flow and hypoxia. No direct relationship between 8-iso-PGF2alpha or 15-keto-dihydro-PGF2alpha and troponin T was evident. The present study adds to the increasingly complex pathophysiological roles of ROS acting both as signal molecules and as mediators of tissue injury.
在接受经皮冠状动脉介入治疗（PCI）的急性心肌梗死（AMI）中，心肌损伤源于缺血和再灌注期间的复杂过程。活性氧（ROS）的释放可能导致累积的心肌损伤。
通过对接受AMI直接PCI的患者外周血进行频繁采样，检测氧化应激和早期炎症反应。其次，评估这些参数与心肌损伤程度之间是否存在相关性。
纳入16例在AMI发作后6小时内接受直接PCI的患者。在手术开始时（t0）以及再灌注后的24小时内反复采集外周血。主要血浆分析指标包括：8-异前列腺素F2α（氧化应激）、15-酮二氢前列腺素F2α（环氧化酶介导的炎症）；以及肌钙蛋白T（心肌损伤）。额外的分析包括：总抗氧化状态（TAS）；维生素；高敏C反应蛋白（hsCRP）和血脂。
血流恢复后8-异前列腺素F2α升高，3小时后恢复到t0值，第二天降至t0值以下。TAS从t0到第二天显著降低。8-异前列腺素F2α与肌钙蛋白T值之间无显著相关性。15-酮二氢前列腺素F2α在第一小时内升高。24小时后hsCRP大幅升高。
AMI患者经直接PCI再灌注后，立即诱导氧化应激和炎症反应。缺血期间8-异前列腺素F2α升高表明，在冠状动脉血流严重减少和缺氧期间也可能产生ROS。8-异前列腺素F2α或15-酮二氢前列腺素F2α与肌钙蛋白T之间未发现明显的直接关系。本研究进一步证明了ROS作为信号分子和组织损伤介质的病理生理作用日益复杂。
