Mikkonen R, Lehto T, Koistinen V, Aronen H J, Kivisaari L, Meri S
Department of Radiology, Helsinki University Central Hospital, Finland.
Scand J Immunol. 1997 Apr;45(4):371-7. doi: 10.1046/j.1365-3083.1997.d01-414.x.
The authors examined the effect of four different kinds of contrast media (ionic/non-ionic, monomer/dimer) on the activation of the complement (C) system (haemolytic activity and anaphylatoxin generation) in vitro. In addition, the authors compared the effect of contrast media on inulin-mediated generation of the anaphylatoxin derivative C3a des Arg in sera from urticarial reactors and their non-reacting controls. It was observed that the incubation of commercial iohexol, ioxaglate, iodixanol and meglumin amidotriz solutions in normal human serum (NHS) resulted in a dose-dependent decrease in the haemolytic activity of the alternative C pathway. Contrary to expectations the contrast media did not activate C in NHS. Instead, inulin-induced generation of C3a des Arg was inhibited by all the four contrast media. The strongest inhibitor was ioxaglate, an ionic dimer. No significant difference between the urticarial reactors and non-reactors in the inhibition of C3a des Arg generation was observed. In analyzing the mechanism of C inhibition we found that the contrast media solutions, particularly the ionic ones, prevented formation of the alternative pathway C3 convertase, C3bBb, by inhibiting the binding of factor B to surface-associated C3b molecules. The results suggest that the previously observed decrease in haemolytic C titres by contrast media is due to direct suppression of C activity rather than activation-induced consumption.
作者研究了四种不同类型的造影剂（离子型/非离子型、单体/二聚体）对体外补体（C）系统激活（溶血活性和过敏毒素生成）的影响。此外，作者比较了造影剂对来自荨麻疹反应者及其非反应对照血清中菊粉介导的过敏毒素衍生物C3a des Arg生成的影响。观察到，将市售的碘海醇、碘克沙醇、碘克酸和葡甲胺泛影溶液在正常人血清（NHS）中孵育，会导致替代补体途径的溶血活性呈剂量依赖性降低。与预期相反，造影剂在NHS中并未激活补体。相反，所有四种造影剂均抑制了菊粉诱导的C3a des Arg生成。最强的抑制剂是离子型二聚体碘克沙醇。在抑制C3a des Arg生成方面，荨麻疹反应者和非反应者之间未观察到显著差异。在分析补体抑制机制时，我们发现造影剂溶液，尤其是离子型造影剂溶液，通过抑制因子B与表面相关C3b分子的结合，阻止了替代途径C3转化酶C3bBb的形成。结果表明，先前观察到的造影剂导致溶血补体滴度降低是由于补体活性的直接抑制，而非激活诱导的消耗。
