Riemann C D, Massey C V, McCarron D L, Borkowski P, Johnson P C, Ziskind A A
Division of Cardiology, University of Maryland, Baltimore.
Am Heart J. 1993 Jan;125(1):71-8. doi: 10.1016/0002-8703(93)90058-h.
Contrast agent-mediated endothelial injury may be clinically relevant to the development of acute thrombosis after coronary interventions. We sought to investigate the extent to which contrast agents increase platelet deposition by measuring deposition of indium-111 radiolabeled platelets in an isolated perfused rabbit carotid artery model. Carotid artery segments were perfused at physiologic temperature, pressure, and shear. Vessels were subjected to angioplasty or no angioplasty before exposure to either buffer, diatrizoate (high osmolal/ionic), ioxaglate (low osmolal/ionic), or ioversol (low osmolal/nonionic). Subsequent deposition of indium-111 radiolabeled platelets was quantified. In vessels without balloon angioplasty, platelet deposition (platelets/cm2) was 110,000 +/- 95,000 for buffer perfused vessels, 280,000 +/- 210,000 for vessels perfused with diatrizoate, 290,000 +/- 160,000 for vessels perfused with ioxaglate, and 130,000 +/- 98,000 for vessels perfused with ioversol. After balloon angioplasty, platelet deposition was 1,300,000 +/- 590,000 for buffer controls, 1,800,000 +/- 320,000 for diatrizoate-perfused vessels, 1,500,000 +/- 450,000 for ioxaglate-perfused vessels, and 1,000,000 +/- 180,000 for ioversol-perfused vessels. In vessels without balloon angioplasty, diatrizoate and ioxaglate increased platelet deposition 2.5-fold and 2.6-fold, respectively, relative to buffer-perfused vessels (p < 0.05 and p < 0.01), whereas no increase was seen with ioversol. After balloon angioplasty, diatrizoate increased platelet deposition 1.4-fold over control (p < 0.05), whereas ioxaglate and ioversol showed no statistically significant increase. We conclude that ionic contrast media may cause more endothelial injury and associated localized platelet deposition than nonionic contrast media. These findings may be relevant to coronary interventions, specifically with regard to acute closure and chronic restenosis.
造影剂介导的内皮损伤在临床上可能与冠状动脉介入治疗后急性血栓形成的发生有关。我们试图通过在离体灌注兔颈动脉模型中测量铟 - 111放射性标记血小板的沉积，来研究造影剂增加血小板沉积的程度。在生理温度、压力和剪切力条件下对颈动脉段进行灌注。在暴露于缓冲液、泛影葡胺（高渗/离子型）、碘克沙醇（低渗/离子型）或碘佛醇（低渗/非离子型）之前，对血管进行或不进行血管成形术。随后对铟 - 111放射性标记血小板的沉积进行定量。在未进行球囊血管成形术的血管中，缓冲液灌注的血管血小板沉积（血小板数/cm²）为110,000±95,000，泛影葡胺灌注的血管为280,000±210,000，碘克沙醇灌注的血管为290,000±160,000，碘佛醇灌注的血管为130,000±98,000。在球囊血管成形术后，缓冲液对照组的血小板沉积为1,300,000±590,000，泛影葡胺灌注的血管为1,800,000±320,000，碘克沙醇灌注的血管为1,500,000±450,000，碘佛醇灌注的血管为1,000,000±180,000。在未进行球囊血管成形术的血管中，相对于缓冲液灌注的血管，泛影葡胺和碘克沙醇分别使血小板沉积增加2.5倍和2.6倍（p<0.05和p<0.01），而碘佛醇未观察到增加。在球囊血管成形术后，泛影葡胺使血小板沉积比对照组增加1.4倍（p<0.05），而碘克沙醇和碘佛醇未显示出统计学上的显著增加。我们得出结论，离子型造影剂可能比非离子型造影剂引起更多的内皮损伤及相关的局部血小板沉积。这些发现可能与冠状动脉介入治疗有关，特别是在急性闭塞和慢性再狭窄方面。
