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首页> 外文期刊>Life sciences >Human thrombocytes are able to induce a myocardial dysfunction in the ischemic and reperfused guinea pig heart mediated by free radicals-role of the GPIIb/IIIa-blocker tirofiban.
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Human thrombocytes are able to induce a myocardial dysfunction in the ischemic and reperfused guinea pig heart mediated by free radicals-role of the GPIIb/IIIa-blocker tirofiban.

机译：人的血小板能够在GPIIb / IIIa阻滞剂替罗非班的自由基作用介导的缺血和再灌注的豚鼠心脏中诱发心肌功能障碍。

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In recent studies, we could demonstrate a myocardial dysfunction induced by homologous platelets in ischemic and reperfused guinea pig hearts. Aim of the current study was to find out whether or not this is a phenomenon specific for platelets isolated from guinea pigs and to further examine the mechanisms of a possible cardiodepressive effect of human platelets. Isolated guinea pig hearts were exposed to a 30 min low-flow ischemia (1 ml/min) and reperfused. Human thrombocytes were administered as bolus (20.000 thrombocytes/&mgr;l perfusion buffer) in the 15(th) min of ischemia or in the 1(st) or 5(th) min of reperfusion in the presence of thrombin. Recovery of external heart work (REHW) and intracoronary platelet retention (RET) were quantified in percent. In additional experiments, the GPIIb/IIIa-blocker tirofiban (10 &mgr;g/ml perfusion buffer) or the radical scavenger superoxide dismutase (SOD-10 U/ml perfusion buffer) were added. Platelet application in the absence of tirofiban, either during ischemia (REHW 75.4 +/- 4%, RET 22.2 +/- 2%) or the 1st min (REHW 71.6 +/- 1%, RET 31.2 +/- 2%) or the 5th min of reperfusion (REHW 63.2 +/- 4%, RET 40.5 +/- 1%) led to a significant reduction of REHW and a significant increase of RET. The coapplication of tirofiban, on the other hand, prevented RET at all three times of platelet application (1.1 +/- 1.7%, 0% or 2.1 +/- 1.2%, respectively). An improvement of REHW, however, could only be noticed during ischemia (89 +/- 2%), whereas coapplication of tirofiban in early (72.9 +/- 3%) or in late reperfusion (74.6 +/- 2%) did not lead to a significant increase of REHW. Coapplication of SOD, on the other hand, significantly improved REHW in early (88.1 +/- 1) or late (95.9 +/- 1) reperfusion but not during ischemia (83.5 +/- 2). Corresponding to REHW, RET was changed significantly by coapplication of SOD during early (1 +/- 2%) or late (0%) reperfusion but not during ischemia (21.1 +/- 4%). We conclude that human thrombocytes are able to induce a myocardial dysfunction in ischemic and reperfused guinea pig hearts mediated by reactive oxygen species and independent of intracoronary platelet adhesion.
机译：在最近的研究中，我们可以证明在缺血和再灌注的豚鼠心脏中由同源血小板引起的心肌功能障碍。本研究的目的是找出这是否是豚鼠分离出的血小板所特有的现象，并进一步研究可能对人血小板产生心脏降压作用的机制。将分离的豚鼠心脏暴露于30分钟的低流量缺血（1 ml / min）并重新灌注。在缺血的第15分钟或凝血酶存在的再灌注的第1（st）或第5（th）分钟内，以大剂量（20.000血小板/ mgl灌注缓冲液）的形式给予人血小板。量化外部心脏功（REHW）和冠状动脉内血小板retention留（RET）的百分比。在另外的实验中，加入GPIIb / IIIa-阻断剂替罗非班（10μg/ ml灌注缓冲液）或自由基清除剂超氧化物歧化酶（SOD-10U / ml灌注缓冲液）。在缺血期间（REHW 75.4 +/- 4％，RET 22.2 +/- 2％）或第一分钟（REHW 71.6 +/- 1％，RET 31.2 +/- 2％）或不存在替罗非班的情况下应用血小板再灌注的第5分钟（REHW 63.2 +/- 4％，RET 40.5 +/- 1％）导致REHW显着降低和RET显着增加。另一方面，替罗非班的共同应用可在所有三次血小板应用（分别为1.1 +/- 1.7％，0％或2.1 +/- 1.2％）时防止RET。然而，仅在缺血期间（89 +/- 2％）可以观察到REHW的改善，而在早期（72.9 +/- 3％）或晚期再灌注（74.6 +/- 2％）的同时应用替罗非班并没有注意到导致REHW大幅增加。另一方面，在早期（88.1 +/- 1）或晚期（95.9 +/- 1）的再灌注中，SOD的联合应用可显着改善REHW，而在缺血期间（83.5 +/- 2）则不能。与REHW相对应，在早期（1 +/- 2％）或晚期（0％）再灌注期间，联合应用SOD可显着改变RET，但在缺血期间（21.1 +/- 4％）则不会。我们得出的结论是，人类血小板能够在由活性氧介导且独立于冠状动脉内血小板粘附的缺血性和再灌注豚鼠心脏中诱导心肌功能障碍。

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