Iodinated contrast media (CM) can potentially cause contrast-induced nephropathy (CIN). It is not clear, however, whether particular types of CM are more prone to cause CIN than others. In this study we compare 4 types of CM (ionic vs. nonionic; monomer vs. dimer) on their effects on the microvessels that supply the area at risk for renal damage in CIN (outer medullary descending vasa recta–DVR).
Material and Methods:
Using microdissection techniques, single DVR were isolated from rats and perfused using a set of concentric pipettes. After stabilization, perfusate was exchanged for a buffered solution containing either vehicle, or amidotrizoate (an ionic/monomeric CM), ioxaglate (an ionic/dimeric CM), iopromide (a nonionic/monomeric CM), and iodixanol (a nonionic/dimeric CM). The final iodine concentration was 23 mg iodine/mL, a concentration similar to that expected for coronary interventions. At this dilution, properties of CM solutions like viscosity and osmolarity are similar to the vehicle solution. To rule out further influence of CM-osmolarity and viscosity, the DVR bath solution was kept isoosmolar to the perfusate. Angiotensin II dose response curves were performed after the 20 minutes of perfusion. Digital videomicroscopy was used for measurements of luminal diameter.
All types of CM reduced luminal diameter of perfused DVR in a similar manner. After 20 minutes of perfusion, size of DVR were: 45% ± 7% of initial diameter for the amidotrizoate-group; 53% ± 6% for the ioxaglate-group; 63% ± 11% for the iopromide-group; and 49% ± 8% for the iodixanol-group. Control group remained at 96% ± 4% of initial diameter. The angiotensin II dose response curves showed greater reactivity for amidotrizoate, iopromide and iodixanol, when compared with controls.
Under conditions where effects of osmolarity and viscosity are kept insignificant, perfusion of DVR using different types of iodinated CM leads to similar constriction of DVR. The response to angiotensin II was enhanced in 3 of the tested CM. This may be an important mechanism in the pathophysiology of CIN.