P. Cipolla et al., EFFECTS OF IODINATED CONTRAST-MEDIA ON PULMONARY AIRWAY-RESISTANCE INANESTHETIZED GUINEA-PIGS, Academic radiology, 2(4), 1995, pp. 306-312
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.