Steg P G, Pasquier C, Huu T P, Chollet-Martin S, Juliard J M, Himbert D, Pocidalo M A, Gourgon R, Hakim J
Service de Cardiology, INSERM U294, Hôpital Bichat, Paris, France.
Eur J Med. 1993 Jan;2(1):6-10.
Percutaneous transluminal coronary angioplasty (PTCA) induces deep arterial wall injury and transient ischaemia. The aim of this study was to demonstrate that PTCA could result in priming or activation of the neutrophils and the complement system.
Blood was drawn from the coronary sinus before and immediately after PTCA in 7 patients and before and immediately after coronary angiography in 7 patients (to ensure that the changes observed after PTCA were not solely related to the angiographic procedure). Neutrophil priming was assessed ex vivo by whole blood chemiluminescence stimulated in vitro by formyl-methionyl-leucyl-phenylalanine, phorbol myristate and opsonized zymosan. Neutrophil activation was assessed by measurement of plasma lactoferrin.
Whole blood chemiluminescence increased after PTCA, regardless of the stimulus used, while it did not after arteriography. After PTCA, lactoferrin increased 2-fold (p < 0.02) whereas after arteriography a non-significant increase was observed. Neutrophil count and adherence properties were not modified by either PTCA or arteriography. Total haemolytic complement (CH50), C3, C4 and B factor decreased slightly (7 to 16%) after both PTCA and arteriography.
Early after PTCA, the neutrophil oxidative response, assessed by stimulated whole blood chemiluminescence, increased, suggesting a "priming" effect of PTCA on neutrophils. In addition, plasma lactoferrin levels increased, indicating neutrophil activation. Finally, there was a mild global activation of the complement system, most likely related to the contrast agent, and which may play a role in the "priming" process. Neutrophil priming and activation may participate in several phenomena occurring after angioplasty such as enhanced vasoconstriction and post-ischaemic myocardial dysfunction. In addition, it may participate in triggering local inflammatory processes.
经皮腔内冠状动脉成形术（PTCA）会导致动脉壁深层损伤和短暂性缺血。本研究的目的是证明PTCA可导致中性粒细胞和补体系统的预激或激活。
在7例患者PTCA前和PTCA后即刻以及7例患者冠状动脉造影前和冠状动脉造影后即刻从冠状窦采血（以确保PTCA后观察到的变化并非仅与血管造影操作有关）。通过体外由甲酰甲硫氨酰亮氨酰苯丙氨酸、佛波酯肉豆蔻酸酯和调理酵母聚糖刺激的全血化学发光来评估中性粒细胞预激。通过测量血浆乳铁蛋白来评估中性粒细胞激活。
无论使用何种刺激，PTCA后全血化学发光均增加，而动脉造影后则未增加。PTCA后，乳铁蛋白增加了2倍（p<0.02），而动脉造影后观察到的增加不显著。中性粒细胞计数和黏附特性均未因PTCA或动脉造影而改变。PTCA和动脉造影后总溶血补体（CH50）、C3、C4和B因子均略有下降（7%至16%）。
PTCA后早期，通过刺激全血化学发光评估的中性粒细胞氧化反应增加，提示PTCA对中性粒细胞有“预激”作用。此外，血浆乳铁蛋白水平升高，表明中性粒细胞激活。最后，补体系统有轻度整体激活，最可能与造影剂有关，且可能在“预激”过程中起作用。中性粒细胞预激和激活可能参与血管成形术后发生的多种现象，如血管收缩增强和缺血后心肌功能障碍。此外，它可能参与触发局部炎症过程。
