EFFECTS OF IODINATED CONTRAST-MEDIA ON PULMONARY AIRWAY-RESISTANCE INANESTHETIZED GUINEA-PIGS

Rationale and Objectives. Bronchospasm is occasionally observed follow ing iodinated X-ray contrast medium administration. We performed an in vivo study in guinea pigs to investigate the effects of a number of i odinated contrast media on pulmonary airway resistance and the mechani sms underlying the potential bronchoconstrictor effect. Methods. The c ontrast media studies were the pharmaceutical formulations of iomeprol (400 mg I/ml), iopamidol (370 mg I/ml), and iohexol (350 mg I/ml), wh ich are nonionic, triiodinated contrast media; diatrizoate (370 mg I/m l) an ionic, triiodinated contrast medium; iotrolan (300 mg I/ml), a n onionic, hexaiodinated contrast medium; and iocarmate (280 mg I/ml) an d ioxaglate (320 mg I/ml), which are both hexaiodinated and ionic cont rast media. Each contrast medium was administered intravenously at 2 g I/kg. Changes in pulmonary airway resistance were evaluated by measur ing intratracheal pressure at the moment of maximum insufflation, or m aximal insufflation pressure (MIP), in anesthetized guinea pigs submit ted to forced ventilation. Results. All contrast media except ioxaglat e caused mean increases of MIP of no more than 20%. By contrast, ioxag late caused a marked bronchoconstrictor effect, increasing MIP by 242% +/- 46%. Of the drugs tested for antagonistic action on this increase in MIP, salbutamol inhibited almost completely the increase in MIP fo r the first 40 min posttreatment. Similarly, lysine acetylsalicylate a nd indomethacin consistently reduced MIP after contrast media administ ration to levels only 30% and 14% above those of baseline precontrast media, respectively. Promethazine had only a minor inhibitory effect, and the response to prednisolone varied. Conclusion. There was no appa rent relationship between the size of the increase in airway resistanc e and the charge or molecular weight of the contrast agent molecule or the pharmaceutical formulation. The increase induced by ioxaglate mus t be attributed to inherent molecular toxicity mediated through a dire ct action on the production of bradykinin and/or the prostanoid produc ts of the cyclooxygenase pathway, rather than through a direct action on the release of histamine.