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介入性热损伤后人体动脉壁的血栓形成倾向

Thrombogenicity of the human arterial wall after interventional thermal injury.

作者信息

Post M J, de Graaf-Bos A N, van Zanten H G, de Groot P G, Sixma J J, Borst C

机构信息

Department of Cardiology, University Hospital Utrecht, The Netherlands.

出版信息

J Vasc Res. 1996 Mar-Apr;33(2):156-63. doi: 10.1159/000159144.

DOI:10.1159/000159144
PMID:8630349
Abstract

Thermal injury has been shown to reduce platelet adhesion (PA) in vitro but not in vivo. The controversy may be based on the mode of thermal injury, the anticoagulation regimen, or species differences. Human and rabbit arteries were dilated by a radio-frequency (RF)-heated balloon (RF dilation) or by immersion in heated buffer. The artery segments were perfused in an annular perfusion chamber with blood anticoagulant by citrate or heparin (37 degrees C, 5 min, shear rate: 1,300 s-1). To determine PA to deep wall layers, 6-micron cross-sections of heated arteries were perfused in a rectangular perfusion chamber (37 degrees C, 5 min, 1,300 s-1). After RF dilation of human arteries at 55 and 90 degrees C, subendothelical PA (citrated blood) decreased from 28.9% at 37 degrees C to 6.8%, and increased to 39.6%, respectively (in both cases p<0.05). Heparin anticoagulation resulted in subendothelial fibrin deposition that was equal after 37 and 90 degrees C, and decreased after 55 degrees C. Heating of cross-sections of atherosclerotic coronary arteries to 55 and 90 degrees C, showed increased and decreased PA, respectively, to the intima and media. No effect was observed on the highly reactive adventitia and atherosclerotic plaque. We conclude that thermal balloon angioplasty at 90 degrees C reduces PA to the arterial subendothelium, but not to the adventitia or the atherosclerotic plaque. As thermal balloon angioplasty in patients will always produce a region with increased PA at 55 degrees C and as heparin anticoagulation permits fibrin deposition that is not affected by heat, it is unlikely that thermal balloon angioplasty alone will reduce thrombotic complications.

摘要

热损伤已被证明在体外可降低血小板黏附(PA),但在体内却不然。这种争议可能基于热损伤的方式、抗凝方案或物种差异。用人和兔的动脉,通过射频(RF)加热球囊(RF扩张)或浸入加热缓冲液来进行扩张。将动脉段置于环形灌注室中,用柠檬酸盐或肝素进行血液抗凝(37℃,5分钟,剪切速率:1300秒⁻¹)。为了确定对动脉深层壁层的PA,将加热动脉的6微米横截面置于矩形灌注室中灌注(37℃,5分钟,1300秒⁻¹)。在55℃和90℃对人动脉进行RF扩张后,内皮下PA(枸橼酸盐抗凝血液)从37℃时的28.9%分别降至6.8%,并升至39.6%(两种情况均p<0.05)。肝素抗凝导致内皮下纤维蛋白沉积,在37℃和90℃后相等,在55℃后减少。将动脉粥样硬化冠状动脉横截面加热至55℃和90℃,分别显示对内膜和中膜的PA增加和减少。对高反应性外膜和动脉粥样硬化斑块未观察到影响。我们得出结论,90℃的热球囊血管成形术可降低对动脉内皮下的PA,但对外膜或动脉粥样硬化斑块则不然。由于患者的热球囊血管成形术总会产生一个55℃时PA增加的区域,并且由于肝素抗凝允许不受热影响的纤维蛋白沉积,仅热球囊血管成形术不太可能减少血栓形成并发症。

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Thrombogenicity of the human arterial wall after interventional thermal injury.介入性热损伤后人体动脉壁的血栓形成倾向
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Interventional thermal injury of the arterial wall: unfolding of von Willebrand factor and its increased binding to collagen after 55 degrees C heating.动脉壁的介入性热损伤:血管性血友病因子的展开及其在55摄氏度加热后与胶原蛋白结合增加。
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Effects of thermal exposure on binding of heparin in vitro to the arterial wall and to clot and on the chronic angiographic luminal response to local application of a heparin film during angioplasty in an in vivo rabbit model.热暴露对体外肝素与动脉壁及血栓结合的影响,以及对体内兔模型血管成形术中局部应用肝素膜的慢性血管造影管腔反应的影响。
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