Oxidative stress and inflammatory response during and following coronary interventions for acute myocardial infarction
Oxidative stress and inflammatory response during and following coronary interventions for acute myocardial infarction
复制标题
DOI：
10.1080/10715760400028027
复制
发表时间：
2005-06-01
影响因子：
3.3
通讯作者：
Wiseth, R
中科院分区：
文献类型：
--
作者：
Berg, K;Jynge, P;Wiseth, R
背景资料。在经皮冠状动脉介入治疗的急性心肌梗死患者中，心肌损伤是缺血和再灌注过程中复杂的过程所致。目的：通过对急性心肌梗死患者急诊直接经皮冠状动脉介入治疗(PCI)患者外周血中氧化应激和早期炎症反应的检测，探讨ROS的释放与心肌损伤的关系。其次，评估这些参数与心肌损伤程度之间是否存在相关性。方法：16例急性心肌梗死发病6h内行直接经皮冠状动脉介入治疗的患者。于手术开始时(TO)和再灌流后24小时内重复采集外周血。主要血浆分析包括：8-iso-PGF(2α)(氧化应激)、15-酮-二氢PGF(2α)(环氧合酶介导的炎症)和肌钙蛋白-T(心肌损伤)。其他分析包括：总抗氧化状态(TAS)；维生素；hsCRP和血脂。结果：8-Iso-PGF(2α)在血流恢复后升高，3h后恢复到正常水平，次日降至以下水平。TAS从一天到第二天显著下降。8-iso-PGF(2α)与肌钙蛋白T值无显著相关性。15-酮-二氢前列腺素F(2α)在1小时内升高。结论：急性心肌梗死直接经皮冠状动脉介入治疗后即刻发生氧化应激和炎症反应。缺血期间8-iso-PGF(2α)的升高表明，在冠状动脉血流量严重减少和缺氧时也可能发生ROS的产生。8-异-前列腺素F(2α)或15酮二氢前列腺素F(2α)与肌钙蛋白T无直接关系。这项研究增加了ROS日益复杂的病理生理作用，它既是信号分子，也是组织损伤的媒介。
Background. 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.Aims: To examine by frequent sampling of peripheral blood oxidative stress and early inflammation inpatients undergoing primary PCI for AMI. Secondly, to assess whether a correlation exists between these parameters and the extent of myocardial damage.Methods: Sixteen patients undergoing primary PCI within 6 h of AMI onset were included. Peripheral blood was sampled at start of procedure (to) and repeatedly over 24 h following reperfusion. Main plasma analyses were: 8-iso-PGF(2 alpha) (oxidative stress), 15-keto-dihydro-PGF(2 alpha) (cyclooxygenase-mediated inflammation); and troponin-T (myocardial injury). Additional analyses included: total antioxidant status (TAS); vitamins; hsCRP and lipids.Results: 8-Iso-PGF(2 alpha) increased following restoration of blood flow, returned to to values after 3 h and was reduced below to the following day. TAS decreased significantly from to to the next day. There was no significant correlation between 8-iso-PGF(2 alpha) and troponin T values. 15-Keto-dihydro-PGF(2 alpha) was elevated during the first hour. There was a major rise in hsCRP after 24 h.Conclusion: Following reperfusion by primary PCI in AMI, oxidative stress and an inflammatory response are induced immediately. A rise in 8-iso-PGF(2 alpha) during ischemia indicate that ROS generation may also take place during severely reduced coronary blood flow and hypoxia. No direct relationship between 8-iso-PGF(2 alpha) or 15-keto-dihydro-PGF(2 alpha) 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.