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首页> 外文期刊>Platelets >A myocardial ischemia-and reperfusion-induced injury is mediated by reactive oxygen species released from blood platelets
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A myocardial ischemia-and reperfusion-induced injury is mediated by reactive oxygen species released from blood platelets

机译：血小板释放出的活性氧介导心肌缺血再灌注损伤

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In recent experimental studies, blood platelets have been found to exhibit some cardiodepressive effects in ischemic and reperfused guinea pig hearts independent of thrombus formation. These effects seemed to be mediated by reactive oxygen species (ROS). However, the source of these ROS-platelets or heart-remained still unknown. Isolated, buffer-perfused and pressure-volume work performing guinea pig hearts were exposed to a low-flow ischemia (1ml/min) of 30 min duration and reperfused at a constant flow of 5th ml/min. Human thrombocytes were administered as 1min bolus (20,000 thrombocytes/μl perfusion buffer) in the 15th min of ischemia or in the 1st or 5th min of reperfusion in the presence of thrombin (0.3U/ml perfusion buffer). Recovery of external heart work (REHW) was expressed as ratio between postischemic and preischemic EHW in percent. Intracoronary platelet retention (RET) was quantified as percent of platelets applied. In a second set of experiments, thrombocytes were incubated with 10μM of the irreversible NADPH oxidase blocker diphenyliodonium chloride and washed twice, thereafter, and administered according to the same protocol as described above. Hearts exposed to ischemia and reperfusion in the presence of thrombin but without application of platelets served as controls. Controls without application of platelets did not reveal a severe compromisation of myocardial function (REHW 85.5±1%). However, addition of platelets during ischemia or in the 1st or 5th min of reperfusion led to a significant reduction of REHW as compared with controls (REHW 62.4±6, 53.9±3, 40.5±3, respectively). Application of platelets pretreated with diphenyliodonium chloride did not reveal any cardiodepressive effects being significantly different from controls without platelet application. Moreover, treatment of platelets with diphenyliodonium chloride did not significantly decrease intracoronary platelet retention. In conclusion, these results demonstrate that cardiodepressive effects of human thrombocytes in ischemic and reperfused guinea pig hearts are mediated by ROS released from thrombocytes and not the heart.
机译：在最近的实验研究中，已经发现血小板在缺血和再灌注的豚鼠心脏中表现出某些心脏抑制作用，而与血栓形成无关。这些作用似乎是由活性氧（ROS）介导的。然而，这些ROS-血小板或心脏残留的来源仍然未知。进行豚鼠心脏分离，缓冲液灌注和按压力量工作，要进行30分钟的低流量缺血（1ml / min），并以5ml / min的恒定流量再灌注。在凝血酶（0.3U / ml灌注缓冲液）存在的情况下，在缺血的第15分钟或在再灌注的第1或第5分钟，以1分钟的剂量（20,000血小板/μl灌注缓冲液）施用人血小板。外部心脏功（REHW）的恢复表示为缺血后和缺血前EHW之间的百分比。冠状动脉内血小板保留（RET）定量为所用血小板的百分比。在第二组实验中，将血小板细胞与10μM不可逆NADPH氧化酶阻滞剂二苯基碘化鎓氯化物一起孵育，并洗涤两次，然后按照上述相同方案进行给药。在凝血酶存在下但未应用血小板的情况下暴露于局部缺血和再灌注的心脏作为对照。不施加血小板的对照未显示出严重的心肌功能损害（REHW 85.5±1％）。然而，与对照组相比，在缺血期间或再灌注的第1或第5分钟加入血小板导致REHW显着降低（分别为REHW 62.4±6、53.9±3、40.5±3）。用二苯碘氯铵预处理的血小板的应用并未显示出与未应用血小板的对照组相比有明显不同的心脏抑制作用。此外，用二苯碘氯化铵处理血小板并没有显着降低冠状动脉内血小板保留。总之，这些结果表明，人血小板在缺血和再灌注的豚鼠心脏中的心脏降压作用是由血小板而非心脏释放的ROS介导的。

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