Hoem N O, Briseid G, Ekelund S, Salvesen S
Acta Pharmacol Toxicol (Copenh). 1986 Sep;59(3):189-94. doi: 10.1111/j.1600-0773.1986.tb00153.x.
Blood pressure (BP), plasma prekallikrein (PK), and the extent of activation of factor XII (XII-ACT) were studied after the intravenous injection into rats of dextran (Macrodex), the ionic radiographic contrast substance iodipamide (Biligrafin), or the non-ionic contrast substance iohexol (Omnipaque). After acetone activation plasma kallikrein was assayed as plasminogen activator, BAEe esterase or S-2302 amidase, and factor XIIa was assayed as kaolin-activated prekallikrein activator. Dextran induced a strong and lasting hypotension, preceded by significant lowerings in PK and XII-ACT. Iodipamide induced a rapid and dose dependent BP fall, no change in plasma PK, but a slightly reduced XII-ACT. Iohexol induced no significant alterations, neither in BP, nor in plasma parameters. Pretreatments of the rats with iodipamide abolished the dextran-induced reductions in PK and XII-ACT, and almost blocked the fall in BP. We conclude that the ionic contrast substance iodipamide is capable of blocking dextran shock in the rat by preventing an activation of the contact activating system in plasma.
在给大鼠静脉注射葡聚糖（Macrodex）、离子型放射造影剂碘达胺（Biligrafin）或非离子型造影剂碘海醇（Omnipaque）后，研究了血压（BP）、血浆前激肽释放酶（PK）以及因子 XII 的激活程度（XII-ACT）。丙酮激活后，将血浆激肽释放酶作为纤溶酶原激活剂、BAEe 酯酶或 S-2302 酰胺酶进行测定，将因子 XIIa 作为高岭土激活的前激肽释放酶激活剂进行测定。葡聚糖诱导强烈且持久的低血压，之前 PK 和 XII-ACT 显著降低。碘达胺诱导快速且剂量依赖性的血压下降，血浆 PK 无变化，但 XII-ACT 略有降低。碘海醇既未引起血压也未引起血浆参数的显著改变。用碘达胺预处理大鼠可消除葡聚糖诱导的 PK 和 XII-ACT 降低，并几乎阻断血压下降。我们得出结论，离子型造影剂碘达胺能够通过阻止血浆中接触激活系统的激活来阻断大鼠的葡聚糖休克。
