| Abstrakt: |
Objective: To determine whether increased elimination of gadobenate ion via the hepatobiliary pathway might compensate for reduced/absent elimination via the urinary pathway in the event of compromised renal function, as a possible protective mechanism against nephrogenic systemic fibrosis (NSF), Methods: 15 male Crl:CD' R(SD)Br rats (Charles River Italia, Como, Italy) randomized to three treatment groups: (1) animals with occluded bile ducts, (2) animals with occluded renal vessels and (3) control animals, each received 0.25 mmol kg-1 of bodyweight of gadobenate dimeglumine (MultiHance'; Bracco Imaging SpA, Milan, Italy). Urine and bile were collected from 0-3 0, 30-60, 60-120, 120-240 and 240-480 min after gadobenate dimeglumine administration prior to exsanguination. Determinations of gadobenate ion in blood, bile and urine were performed by high-performance liquid chromatography. Gadolinium (Gd3 1) levels in excised liver and kidneys were determined by X-ray fluorescence. Results: The recovery of gadobenate ion in the urine of rats with bile duct occlusion was significantly higher than that in the urine of normal rats (89.1 ± 4.2% vs 60.6 ± 2.8%; p< 0.0001). Conversely, mean recovery in the bile of rats with renal vessel occlusion was significantly higher than that in the bile of normal rats (96.16 ±0.55% vs 33.5 ± 4.7%; p < 0.0001). Gadobenate ion was not quantifiable in any group 8h post-injection. Conclusion: Compensatory elimination may be an effective means to overcome compromised renal or hepatobiliary elimination. Advances in knowledge: The absence of NSF in at-risk patients administered with gadobenate dimeglumine may in part reflect greater Gd3+ elimination via the hepatobiliary route. [ABSTRACT FROM AUTHOR] |
